Malaria fever is a disease caused by the cytoxoic protozoon, Plasmodium spp. This parasite is transmitted by an infected female Anopheles mosquito during a blood meal. There are four types of Plasmodium spp viz; Plasmodium falciparum (causes malignant tertian malaria), Plasmodium vivax (causes benign tertian malaria), Plasmodium malariae (causes quartan tertian malaria) and Plasmodium ovale (causes ovala tertian malaria). The main factors which influence the epidermology of malaria are; the intensity of transmission and the immune response of the infected person. Blood smear or film stained with Leishmans stain ,Giemsa’s stain or Field’s stain helps to indentify the parasite.
Life cycle of Plasmodium spp is very distinct in both the infected female Anopheles mosquito and man. The tissue phase comprises the pre-erythrocytic stage which occurs in the liver. The pre-erythrocytic schizonts leave ruptured liver cells and transforms to merozoites which enters the erythrocytes immediately inorder to remain alive.
The large number of merozoites overpowers the lymphocytes (soldiers of the immune system) and attack the erythrocytes. The merozoites develop into trophozoites. The trophozoites are characterized by a ringed type of cytoplasm with a chromatin dot. These trophozoites multiply rapidly and migrate to the bone marrow, spleen, liver and brain. Schizogamy occurs and the rupturing of the affected cells results in the fever.
The gametophyte stage results from some of the merozoites that did not develop into schizonts. They begin the sexual cycle in the mosquito. They become a zygote and transforms into ookinete. Ookinete develops into oocyst and thereafter sporocyst. These sporocysts move to the proboscis as developed sporozoites. Man becomes infected when the mosquito takes a blood meal.
Symptoms include general body weakness especially the joints, increased body temperature, anaemia, splenomegaly and so on. Malaria is a serious disease in subtropical Africa that results in loss of life and decreased productivity. Pregnant women can suffer miscarriage as a result of malaria fever.
Measures taken to prevent and control malaria include; avoiding mosquito bites via the use of mosquito repellant cream, use of mosquito treated nets, preventing the breeding of mosquito larvae.
Treatment of malaria include the use of antimalarials such as chloroquine, Fansidar, Halofantrine, Metakelfin and so on. These drugs contain sulphadozine (500mg) and pyrimethimine (25mg). However, with the development of chloroquine resistance, new and more effective antimalarials are now in use. Examples include Artesunate, Coarten, Lonart and so on.
The development of a malaria vaccine would go a long way in eradicating malaria. Nevertheless, the vaccine that would be developed should be able to attack the trophozoite ,gametophyte and schizont stages of Plasmodium spp. If this medical breakthrough is achieved, the burden of this debilitating global disease would be solved.
Sunday, December 20, 2009
DNA FINGERPRINTING AND ITS MEDICAL IMPORTANCE
A DNA fingerprint is the pattern of fragmented DNA molecules obtained from electrophoresis. Restriction enzymes are used to cleave DNA molecules into specific fragments that can easily be analyzed. Examples of restriction enzymes include EcoR1 , mst II ,Alu I ,Taq I and so on. DNA fingerprinting is also called DNA typing or DNA profiling and is based on sequence polymorphisms.
Variations that occur in the pattern of restriction fragments produced by the same restriction enzyme from DNA of different individuals of same species is termed restriction fragment length polymorphisms (RFLPs). RFLP analysis is therefore invaluable in Forensic Medicine and in screening for mutations and genetic diseases such as sickle cell anaemia.
In Forensic Medicine, restriction fragment length polymorphism analysis can distinguish one individual from millions of people. DNA obtained from congealed blood ,hair follicles and seminal fluid can be used to catch culprits in criminal investigations such as murder, rape, and theft respectively.
The use of techniques such as complementary DNA radiolabeled probes , southern transfer technique, and restriction enzymes are very essential in detecting and screening for mutations and genetic diseases.
The detection of RFLPs utilizes a specialized hybridization technique termed Southern Blotting or Southern Transfer. DNA fragments from digestion of genomic DNA by restriction endonucleases or enzymes by size (in kilobases) electrophoretically. These fragments are denatured by soaking the agarose gel in alkali, and then blotted onto a nylon membrane to reproduce the distribution of fragments in the gel. The membrane is then placed in a solution containing a radioactively labeled DNA probe. Autoradiography is then used to reveal the fragments to which the radiolabeled DNA probe hybridizes.
It is pertinent to note that the number of repeated units in these DNA regions differs in humans (except between identical twins.). Combining the use of several radiolabeled probes makes DNA fingerprinting so selective that it gives accurate results.
However ,the southern transfer technique requires relatively fresh DNA samples and larger amounts of DNA are generally present at a crime scene. RFLP analysis sensitivity is complemented by the use of polymerase chain reaction (PCR) which helps to amplify small amounts of DNA. Forensic investigators can easily obtain DNA from hair follicle, congealed blood ,seminal fluid ,vaginal secretions from victims and suspects to carry out their investigations. Accurate results can be obtained from samples that have stayed for months or even years.
Results obtained from DNA profiling have been useful in convicting criminals and acquitting suspects. Murder mysteries have been solved and paternity disputes have been amicably resolved. An interesting discovery that was achieved with DNA fingerprinting was the discovery and indentification of the bones of the last Russian Czar and his family who were assassinated in 1918 by Forensic investigators in 1996.
Variations that occur in the pattern of restriction fragments produced by the same restriction enzyme from DNA of different individuals of same species is termed restriction fragment length polymorphisms (RFLPs). RFLP analysis is therefore invaluable in Forensic Medicine and in screening for mutations and genetic diseases such as sickle cell anaemia.
In Forensic Medicine, restriction fragment length polymorphism analysis can distinguish one individual from millions of people. DNA obtained from congealed blood ,hair follicles and seminal fluid can be used to catch culprits in criminal investigations such as murder, rape, and theft respectively.
The use of techniques such as complementary DNA radiolabeled probes , southern transfer technique, and restriction enzymes are very essential in detecting and screening for mutations and genetic diseases.
The detection of RFLPs utilizes a specialized hybridization technique termed Southern Blotting or Southern Transfer. DNA fragments from digestion of genomic DNA by restriction endonucleases or enzymes by size (in kilobases) electrophoretically. These fragments are denatured by soaking the agarose gel in alkali, and then blotted onto a nylon membrane to reproduce the distribution of fragments in the gel. The membrane is then placed in a solution containing a radioactively labeled DNA probe. Autoradiography is then used to reveal the fragments to which the radiolabeled DNA probe hybridizes.
It is pertinent to note that the number of repeated units in these DNA regions differs in humans (except between identical twins.). Combining the use of several radiolabeled probes makes DNA fingerprinting so selective that it gives accurate results.
However ,the southern transfer technique requires relatively fresh DNA samples and larger amounts of DNA are generally present at a crime scene. RFLP analysis sensitivity is complemented by the use of polymerase chain reaction (PCR) which helps to amplify small amounts of DNA. Forensic investigators can easily obtain DNA from hair follicle, congealed blood ,seminal fluid ,vaginal secretions from victims and suspects to carry out their investigations. Accurate results can be obtained from samples that have stayed for months or even years.
Results obtained from DNA profiling have been useful in convicting criminals and acquitting suspects. Murder mysteries have been solved and paternity disputes have been amicably resolved. An interesting discovery that was achieved with DNA fingerprinting was the discovery and indentification of the bones of the last Russian Czar and his family who were assassinated in 1918 by Forensic investigators in 1996.
HAEMOGLOBINOPATHIES-PATHOGENESIS AND MANAGEMENT
Haemoglobins are globular proteins found in red blood cells. They are able to bind molecular oxygen and transport oxygen through the lungs and other blood vessels in the body. Haemoglobin variants include;haemoglobin A, haemoglobin S, haemoglobin C, haemoglobin D, haemoglobin E and haemoglobin F (fetal haemoglobin).
Haemoglobinopathies are genetic disorders or abnormalities which result in abnormal structure of one of the globin chains of the haemoglobin molecule. Also ,low levels of synthesis of the normal polypeptide chains (i.e alpha and beta) and production of abnormal chains(i.e delta and epsilon ) result in haemoglobinopathy. These disorders result in thalassemias (alpha and beta), haemoglobin S (Hb S) disease ,haemoglobin C (Hb C) disease, haemoglobin D (Hb D ) disease, and haemoglobin E (Hb E) disease.
Alpha thalassemia results from genetic deletion and this occurs because the α-globin genes are duplicated. This results in unequal crossing over between adjacent α-alleles. Beta thalassemia results from mutations that produces frameshift in the β-globin coding sequence. Studies reveal that majority of β-thalassemias result from mutations affecting the biosynthesis of β-globin mRNA. Thalassemias are classified as major, minor, and intermediate respectively.
Haemoglobin A is the normal haemoglobin found in humans. Two subgroups exists viz; HbA1 and HbA2. The polypeptide chain composition of both HbA1 and HbA2 are α2β2 and α2δ2 respectively. This type of haemoglobin is found in normal shaped erythrocytes and do not possess pathological problem.
In haemoglobin S , there is a replacement of the amino acid glutamic acid with valine at the sixth position in the β-chain. In haemoglobin C, the replacement of the amino acid glutamine with lysine occurs at the sixth position of the β-globin chain. It is pertinent to note that HbC exhibits less haemolysis than HbS. Both HbS and HbC mutant haemoglobins are commonly found among certain black African population. Individuals with HbSC disorder will have an intermediate anaemia from that observed for HbSS. HbSS individuals suffer from sickle cell disease. It is characterized by sickle-shaped erythrocytes, formation of tactoid structure. Victims experience trauma and crises, and require blood transfusions.
HbAS individuals possess the sickling trait but do not suffer from sickle cell disease. However ,when two HbAS individuals marry, they are likely to produce an offspring with the HbSS genetic combination ( i.e a sickler )
Studies reveal that disease conditions associated with these disorders include splenomegaly, haemolytic anaemia, urobilinuria, jaundice and so on.
Management of these disorders include the use of blood transfusion coupled with desferoxamine, folic acid supplement, use of hypoxurea and bone marrow transplantation. HbAS individuals should be discouraged from marrying other HbAS individuals.
Haemoglobinopathies are genetic disorders or abnormalities which result in abnormal structure of one of the globin chains of the haemoglobin molecule. Also ,low levels of synthesis of the normal polypeptide chains (i.e alpha and beta) and production of abnormal chains(i.e delta and epsilon ) result in haemoglobinopathy. These disorders result in thalassemias (alpha and beta), haemoglobin S (Hb S) disease ,haemoglobin C (Hb C) disease, haemoglobin D (Hb D ) disease, and haemoglobin E (Hb E) disease.
Alpha thalassemia results from genetic deletion and this occurs because the α-globin genes are duplicated. This results in unequal crossing over between adjacent α-alleles. Beta thalassemia results from mutations that produces frameshift in the β-globin coding sequence. Studies reveal that majority of β-thalassemias result from mutations affecting the biosynthesis of β-globin mRNA. Thalassemias are classified as major, minor, and intermediate respectively.
Haemoglobin A is the normal haemoglobin found in humans. Two subgroups exists viz; HbA1 and HbA2. The polypeptide chain composition of both HbA1 and HbA2 are α2β2 and α2δ2 respectively. This type of haemoglobin is found in normal shaped erythrocytes and do not possess pathological problem.
In haemoglobin S , there is a replacement of the amino acid glutamic acid with valine at the sixth position in the β-chain. In haemoglobin C, the replacement of the amino acid glutamine with lysine occurs at the sixth position of the β-globin chain. It is pertinent to note that HbC exhibits less haemolysis than HbS. Both HbS and HbC mutant haemoglobins are commonly found among certain black African population. Individuals with HbSC disorder will have an intermediate anaemia from that observed for HbSS. HbSS individuals suffer from sickle cell disease. It is characterized by sickle-shaped erythrocytes, formation of tactoid structure. Victims experience trauma and crises, and require blood transfusions.
HbAS individuals possess the sickling trait but do not suffer from sickle cell disease. However ,when two HbAS individuals marry, they are likely to produce an offspring with the HbSS genetic combination ( i.e a sickler )
Studies reveal that disease conditions associated with these disorders include splenomegaly, haemolytic anaemia, urobilinuria, jaundice and so on.
Management of these disorders include the use of blood transfusion coupled with desferoxamine, folic acid supplement, use of hypoxurea and bone marrow transplantation. HbAS individuals should be discouraged from marrying other HbAS individuals.
GLUT TRANSPORTERS AND DISEASES
Glut protein family mediate glucose transport or uptake in a wide variety of cells. The term “GLUT” is derived from glucose transporter. They are facilitative hexose transporters. GLUT transporters are uniport systems (i.e they transport only one solute such as glucose and other hexoses such as fructose.)
Glut proteins encourage cellular glucose uptake in cells and tissues where they are found. These facilitative glucose transporters form special selective pathways between three major pools of glucose viz; the blood ,the extracellular fluids and the cellular cytoplasm. Most GLUT isoforms have been cloned using techniques such as polymerase chain reaction, reverse transcriptase ,and complementary DNA.
Detailed research reveals that GLUT transporters possess the following characteristics; they possess a putative 12 transmembrane domains with both the amino (NH3+) and carboxyl (COO-) ends inside the membrane, several isoforms have been identified with the designation GLUT1, GLUT2, GLUT3, GLUT4, GLUT5, and up to GLUT 12, possess identical genome SLC2A, are expressed in a tissue and cell specific manner, and they exhibit distinct kinetic and regulatory properties that reflect their roles in cells where they are expressed.
GLUT1 (SLC2A1) is a highly expressed isoform present in almost all cells, contain 492 amino acids and a reduction in blood glucose makes GLUT1 proteins readily available, and this encourages increased flux of glucose across the blood-brain barrier, GLUT2 (SLC2A2) is expressed in hepatocytes, pancreatic β-cells, and so on. GLUT 2 has 524 amino acids. GLUT3 (SLC2A3) is found in neurons and contains 496 amino acids.
GLUT4 (SLC2A4) is expressed in adipocytes and myocytes. GLUT4 has 509 amino acids and is responsible for glucose transport in insulin-sensitive tissues. GLUT 5 (SLC2A5) is a fructose transporter found in the plasma membrane of mature spermatozoa with 501 amino acids. Sperm cells utilize fructose in seminal fluid.
GLUT6 (SLC2A6) has been found in spleen, leukocytes and brain respectively with 507 amino acids.
GLUT7 (SLC2A7) is expressed in liver microsomes and contain 528 amino acids. It encourages diffusion of free glucose in gluconeogenic tissues. GLUT8 (SLC2A8) is expressed in testis, spleen, skeletal muscle and adipose tissues. GLUT8 has 477 amino acids. GLUT9 (SLC2A9) is found expressed in the liver and kidney, has between 511 and 540 amino acids.
GLUT10 (SLC2A10) is expressed in the liver and pancreas and contains 541 amino acids. GLUT11 (SLC2A11) is found in heart and skeletal muscles. It can transport fructose and contain 496 amino acids. GLUT12 (SLC2A12) is expressed in skeletal myocytes, adipocytes and small intestine. GLUT12 encodes 617 amino acids.
Studies show that there is a correlation between GLUT transporters malfunction and diseases. GLUT2 isoform has been implicated in insulin dependent diabetes mellitus. The reason is that this isoform is present in the β-cells of the pancreas where it regulates influx of glucose through insulin secretion. Derangements in glucose homeostasis as regards GLUT4 malfunction is also linked to insulin dependent diabetes mellitus. GLUT 4 is expressed in insulin-sensitive tissues such as myocytes and adipocytes. GLUT10 has been associated with non-insulin dependent diabetes mellitus.
The link between GLUT expression and cancer has been established. Studies involving the use of tec hniques such as reverse transcriptase, polymerase chain reaction, Northern blot analysis and immunochemistry and so on have been able to detect GLUT messenger RNA (mRNA) in sarcomas and carcinomas. Hence ,in cancerous tissues ,there is an abnormal or over-expression of GLUT isoforms especially GLUT1. However ,some tumour cells express specific GLUT mRNA.
Glut proteins encourage cellular glucose uptake in cells and tissues where they are found. These facilitative glucose transporters form special selective pathways between three major pools of glucose viz; the blood ,the extracellular fluids and the cellular cytoplasm. Most GLUT isoforms have been cloned using techniques such as polymerase chain reaction, reverse transcriptase ,and complementary DNA.
Detailed research reveals that GLUT transporters possess the following characteristics; they possess a putative 12 transmembrane domains with both the amino (NH3+) and carboxyl (COO-) ends inside the membrane, several isoforms have been identified with the designation GLUT1, GLUT2, GLUT3, GLUT4, GLUT5, and up to GLUT 12, possess identical genome SLC2A, are expressed in a tissue and cell specific manner, and they exhibit distinct kinetic and regulatory properties that reflect their roles in cells where they are expressed.
GLUT1 (SLC2A1) is a highly expressed isoform present in almost all cells, contain 492 amino acids and a reduction in blood glucose makes GLUT1 proteins readily available, and this encourages increased flux of glucose across the blood-brain barrier, GLUT2 (SLC2A2) is expressed in hepatocytes, pancreatic β-cells, and so on. GLUT 2 has 524 amino acids. GLUT3 (SLC2A3) is found in neurons and contains 496 amino acids.
GLUT4 (SLC2A4) is expressed in adipocytes and myocytes. GLUT4 has 509 amino acids and is responsible for glucose transport in insulin-sensitive tissues. GLUT 5 (SLC2A5) is a fructose transporter found in the plasma membrane of mature spermatozoa with 501 amino acids. Sperm cells utilize fructose in seminal fluid.
GLUT6 (SLC2A6) has been found in spleen, leukocytes and brain respectively with 507 amino acids.
GLUT7 (SLC2A7) is expressed in liver microsomes and contain 528 amino acids. It encourages diffusion of free glucose in gluconeogenic tissues. GLUT8 (SLC2A8) is expressed in testis, spleen, skeletal muscle and adipose tissues. GLUT8 has 477 amino acids. GLUT9 (SLC2A9) is found expressed in the liver and kidney, has between 511 and 540 amino acids.
GLUT10 (SLC2A10) is expressed in the liver and pancreas and contains 541 amino acids. GLUT11 (SLC2A11) is found in heart and skeletal muscles. It can transport fructose and contain 496 amino acids. GLUT12 (SLC2A12) is expressed in skeletal myocytes, adipocytes and small intestine. GLUT12 encodes 617 amino acids.
Studies show that there is a correlation between GLUT transporters malfunction and diseases. GLUT2 isoform has been implicated in insulin dependent diabetes mellitus. The reason is that this isoform is present in the β-cells of the pancreas where it regulates influx of glucose through insulin secretion. Derangements in glucose homeostasis as regards GLUT4 malfunction is also linked to insulin dependent diabetes mellitus. GLUT 4 is expressed in insulin-sensitive tissues such as myocytes and adipocytes. GLUT10 has been associated with non-insulin dependent diabetes mellitus.
The link between GLUT expression and cancer has been established. Studies involving the use of tec hniques such as reverse transcriptase, polymerase chain reaction, Northern blot analysis and immunochemistry and so on have been able to detect GLUT messenger RNA (mRNA) in sarcomas and carcinomas. Hence ,in cancerous tissues ,there is an abnormal or over-expression of GLUT isoforms especially GLUT1. However ,some tumour cells express specific GLUT mRNA.
IODINE REQUIREMENT AND GOITRE
Iodine is one of the halogens. It is one of the essential micronutrients needed by humans. The body contains 20-50mg of iodine and is an essential component of the secretions of the thyroid gland. The thyroid gland synthesizes, stores and secretes the thyroid hormones thyroxine,T4 and tri-iodothyronine,T3. The rate of synthesis and secretion of thyroid hormones are controlled by the pituitary gland. Thyroxine (T4) and tri-iodothyronine (T3) regulate oxygen consumption and heat production including a wide range of metabolic processes. They are also essential for normal growth and development. Iodine after peroxidation, becomes attached to tyrosine residues of thyroglobulin.
Food sources rich in iodine include sea foods such as crayfish, oyster, prawn, lobster and crabs, seeds, eggs, dairy products, cereals. Consumption of iodine is highly variable in different parts of the World.
The minimum requirement for adults has been estimated at 50-75µg/day. Children and mothers require more. Studies have shown that people who live in mountainous regions suffer from iodine deficiency because the soil contain little quantity of iodine. Hence, local produce have little iodine content .Such people suffer from endemic goiter. Endemic goitre results from low levels of thyroid hormones. Endemic goitre is characterized by enlarged thyroid gland.
The development of iodine deficiency can be averted through these methods viz; the addition of potassium iodate to salt used in cooking or in bread (i.e food fortification).In long standing goitre, the use of tyrosine treatment (9.3µg/day) yields appreciable results. Foods rich in gutrogens should be avoided. Examples of such foods are turnips and cabbages.
Iodine toxicity results when doses exceeding the normal daily requirement are administered. The addition of potassium iodate to food for the prophylaxis to endemic goitre is not devoid of hazards if overdose are added. In studies involving animal models, excessive amounts have been shown to inhibit thyroid hormone synthesis. Thyroid necrosis has also been reported.
Food sources rich in iodine include sea foods such as crayfish, oyster, prawn, lobster and crabs, seeds, eggs, dairy products, cereals. Consumption of iodine is highly variable in different parts of the World.
The minimum requirement for adults has been estimated at 50-75µg/day. Children and mothers require more. Studies have shown that people who live in mountainous regions suffer from iodine deficiency because the soil contain little quantity of iodine. Hence, local produce have little iodine content .Such people suffer from endemic goiter. Endemic goitre results from low levels of thyroid hormones. Endemic goitre is characterized by enlarged thyroid gland.
The development of iodine deficiency can be averted through these methods viz; the addition of potassium iodate to salt used in cooking or in bread (i.e food fortification).In long standing goitre, the use of tyrosine treatment (9.3µg/day) yields appreciable results. Foods rich in gutrogens should be avoided. Examples of such foods are turnips and cabbages.
Iodine toxicity results when doses exceeding the normal daily requirement are administered. The addition of potassium iodate to food for the prophylaxis to endemic goitre is not devoid of hazards if overdose are added. In studies involving animal models, excessive amounts have been shown to inhibit thyroid hormone synthesis. Thyroid necrosis has also been reported.
URIC ACID AND ITS CLINICAL CORRELATIONS
Uric acid is the end product of purines and nucleic acid metabolism in man. Uric acid emanates from two routes; from oxidation of purine moieties of degraded nucleic acids (i.e Ribonucleic and deoxyribonucleic acids),from glycine via a direct pathway not involving nucleic acid. Uric acid is filtered by glomerulli and both reabsorped and secreted by the renal tubules. Reasons for requesting uric acid assay include; suspected gout and uric acid nephropathy, renal failure.
Total daily output of uric acid depends partly on the purine content of the diet. Uric acid excretion is diminished when the diet has low purine content, low protein content. Normal levels of serum uric acid is 1-5mg/100ml and it rises to between 8-15mg/100ml in Gout. Diseases such as leukaemia, myeproliferative disorders, plasma cell myeloma and severe haemolytic anaemia, there is considerable breakdown of nuclei of leukocytes. This ultimately results in elevated serum uric acid level.
Gout is a chronic disorder of purine degradation. Types include ; acute gout and chronic gout. Features of gout is as follows viz; hyperuricemia, deposits of sodium monourates in the articular structures, and recurring attacks of acute arthritis with deposits of crystals of monosodium urate in and around the structures the affected joint.
Treatment of gout include the following; restrict the consumption of organ meats since these are rich in purines. Acute gout is treated with drugs such as colchine, phenylbutazone and indomethacin.Chronic gout is characterized by increased excretion of uric acid can be treated with drugs that discourage reabsorption of urates. Drugs such as probenecid (Benemid) and salicylates. Allopurinol inhibits the enzyme xanthine oxidase and this ultimately reduces uric acid synthesis.
Increased secretion of uric acid lowers serum uric acid levels in as much as reabsorption by the renal tubules is not encouraged.
Total daily output of uric acid depends partly on the purine content of the diet. Uric acid excretion is diminished when the diet has low purine content, low protein content. Normal levels of serum uric acid is 1-5mg/100ml and it rises to between 8-15mg/100ml in Gout. Diseases such as leukaemia, myeproliferative disorders, plasma cell myeloma and severe haemolytic anaemia, there is considerable breakdown of nuclei of leukocytes. This ultimately results in elevated serum uric acid level.
Gout is a chronic disorder of purine degradation. Types include ; acute gout and chronic gout. Features of gout is as follows viz; hyperuricemia, deposits of sodium monourates in the articular structures, and recurring attacks of acute arthritis with deposits of crystals of monosodium urate in and around the structures the affected joint.
Treatment of gout include the following; restrict the consumption of organ meats since these are rich in purines. Acute gout is treated with drugs such as colchine, phenylbutazone and indomethacin.Chronic gout is characterized by increased excretion of uric acid can be treated with drugs that discourage reabsorption of urates. Drugs such as probenecid (Benemid) and salicylates. Allopurinol inhibits the enzyme xanthine oxidase and this ultimately reduces uric acid synthesis.
Increased secretion of uric acid lowers serum uric acid levels in as much as reabsorption by the renal tubules is not encouraged.
VITAMINS AND THEIR MEDICAL RELEVANCE
Vitamins are nutritional requirements needed in small amounts by animals for healthy living. Vitamins are classified into 2 groups; water-soluble vitamins and fat-soluble vitamins. Examples of water-soluble vitamins are vitamin C (ascorbic acid) and the B vitamins(i.e vitamin B1,vitamin B2,vitamin B6 and vitamin B12). Fat-soluble vitamins include vitamin A, vitamin D, vitamin E and vitamin K.
Water-soluble vitamins have diverse chemical structures and are polar molecules. They can be synthesized by plants and are therefore provided by food sources such as legumes, whole grains, green leafy vegetables , yeast ,meat and milk. Water-soluble vitamins serves as co-factors (co-enzymes) in enzymatic reactions.
With the exception of vitamin B12 (cyanocobalamin),water-soluble vitamins are not stored in the body. Continuous intake in the diet is required. The human liver can store vitamin B12. They are absorbed in the water along the gastrointestinal tract and are excreted easily along with urine.
Water-soluble vitamins occur in interrelated biochemical pathways and deficiency diseases caused by lack of a single vitamin is rare. Generally ,lack of water-soluble vitamins affect tissues that are growing or metabolizing rapidly such as skin, blood, the digestive tract and the nervous system.
Symptoms of their deficiency include dermatitis, beri-beri, anaemia ,pellagra ,digestive and neurologic disorders. Ascorbic acid (vitamin C) is liable to heat including other water-soluble vitamins. Other important B vitamins include pantothenic acid (vitamin B5), biotin, folic acid (pteroylglutamic acid).
Fat-soluble vitamins are absorbed along with fats in the body. Hence, any substance or factor that favours the absorption of fats and lipids would aid their absorption. Fat-soluble vitamins include vitamin A, vitamin D, vitamin E and vitamin K respectively.
Vitamins A is derived from the precursor beta carotene. Cleavage at the centre of the structure produces retinol. It functions as a hormone. Food sources include fish liver oils, whole milk, carrots and sweet potatoes. Deficiency of retinol results in a variety of symptoms such as dryness of skin, eyes, mucous membranes and night blindness.
Vitamin D is one of the isoprenoid compounds. It exists in diverse forms such as cholecalciferol(vitamin D3),ergocalciferol (vitamin D2). Vitamin D3 is the precursor of 1,25-dihydroxycholecalciferol,a hormone that regulates calcium metabolism. Deficiency of vitamin D results in rickets and bone diseases such as osteomalacia,osteoporosis.
Vitamin E is also referred to as tocopherol. Vitamin E associates with cell membranes, lipid deposits and blood lipoproteins. They serve as biological anti-oxidants. Dietary sources include eggs and vegetable oil. Deficiency of vitamin E results in scaly skin, muscular weakness, and fragile erythrocytes.
Vitamin K has subgroups such as vitamin K1 (phylloquinone) and vitamin K2 (menaquinone). Vitamin K possess an aromatic ring. Detailed research discovered vitamin K as a required factor for blood clotting. Deficiency of vitamin K results in avitaminosis. Steatorrhea and biliary system disorders can result in malabsorption of the fat-soluble vitamins.
Vitamins are essential nutritional requirements required in the life processes of humans. Hence ,fat-soluble vitamins should be consumed with care since they can accumulate in the body to cause metabolic problems. Water-soluble vitamins should be continuously supplied in the diet.
Water-soluble vitamins have diverse chemical structures and are polar molecules. They can be synthesized by plants and are therefore provided by food sources such as legumes, whole grains, green leafy vegetables , yeast ,meat and milk. Water-soluble vitamins serves as co-factors (co-enzymes) in enzymatic reactions.
With the exception of vitamin B12 (cyanocobalamin),water-soluble vitamins are not stored in the body. Continuous intake in the diet is required. The human liver can store vitamin B12. They are absorbed in the water along the gastrointestinal tract and are excreted easily along with urine.
Water-soluble vitamins occur in interrelated biochemical pathways and deficiency diseases caused by lack of a single vitamin is rare. Generally ,lack of water-soluble vitamins affect tissues that are growing or metabolizing rapidly such as skin, blood, the digestive tract and the nervous system.
Symptoms of their deficiency include dermatitis, beri-beri, anaemia ,pellagra ,digestive and neurologic disorders. Ascorbic acid (vitamin C) is liable to heat including other water-soluble vitamins. Other important B vitamins include pantothenic acid (vitamin B5), biotin, folic acid (pteroylglutamic acid).
Fat-soluble vitamins are absorbed along with fats in the body. Hence, any substance or factor that favours the absorption of fats and lipids would aid their absorption. Fat-soluble vitamins include vitamin A, vitamin D, vitamin E and vitamin K respectively.
Vitamins A is derived from the precursor beta carotene. Cleavage at the centre of the structure produces retinol. It functions as a hormone. Food sources include fish liver oils, whole milk, carrots and sweet potatoes. Deficiency of retinol results in a variety of symptoms such as dryness of skin, eyes, mucous membranes and night blindness.
Vitamin D is one of the isoprenoid compounds. It exists in diverse forms such as cholecalciferol(vitamin D3),ergocalciferol (vitamin D2). Vitamin D3 is the precursor of 1,25-dihydroxycholecalciferol,a hormone that regulates calcium metabolism. Deficiency of vitamin D results in rickets and bone diseases such as osteomalacia,osteoporosis.
Vitamin E is also referred to as tocopherol. Vitamin E associates with cell membranes, lipid deposits and blood lipoproteins. They serve as biological anti-oxidants. Dietary sources include eggs and vegetable oil. Deficiency of vitamin E results in scaly skin, muscular weakness, and fragile erythrocytes.
Vitamin K has subgroups such as vitamin K1 (phylloquinone) and vitamin K2 (menaquinone). Vitamin K possess an aromatic ring. Detailed research discovered vitamin K as a required factor for blood clotting. Deficiency of vitamin K results in avitaminosis. Steatorrhea and biliary system disorders can result in malabsorption of the fat-soluble vitamins.
Vitamins are essential nutritional requirements required in the life processes of humans. Hence ,fat-soluble vitamins should be consumed with care since they can accumulate in the body to cause metabolic problems. Water-soluble vitamins should be continuously supplied in the diet.
ZINC AND ITS MEDICAL RELEVANCE
Zinc is an essential trace element element found in humans. It is one of the transition metals found in the periodic table. Zinc is found in the muscle (65% content). However ,higher concentrations are found in the integumental tissues (i.e skin, hair and nails),the retina and the male reproductive organs. The average adult body contains between 10-15mg of zinc.
Richest sources of dietary zinc include whole grains(germs),seeds, nuts, eggs and leafy vegetables, shellfish, dairy products. Zinc is not really stored and is readily lost from the body through faeces, sweating, urine, menstruation. During tissue metabolism and repair, the amount of zinc excreted is greatly increased.
Zinc plays essential role in DNA synthesis and cell division, a constituent of many dehydrogenase enzymes, erythrocyte carbonic anhydrase (essential for acid-base balance).anti-oxidant enzymes such as superoxide dismutase (SOD) which mops up free reactive oxygen species that are cell destructive. Zinc is involved in the binding of insulin within the beta cells of Islets of Langerhans, necessary for male reproductive functions and spermatogenesis especially in the production of testosterone by the Leydig cells. Collagen synthesis and degradation is facilitated by collaginase, a zinc-dependent enzyme.
Zinc deficiency can result in thymic atrophy. Studies have also revealed that symptoms of growth retardation, skin lesions and impaired sexual development was observed in adolescent malnourished boys in Iran and Egypt and was traced to their consumption of phytate bread. Acrodermatitis enteroparthica with symptoms of severe skin lesions, diarrhea ,loss of hair (alopedica) and mental disturbances result from zinc deficiency.
Research has shown that zinc plays a significant role in skin and connective tissue metabolism. The Greeks used Calamine solution on the skin to treat disorders. Zinc, usually in the form of insoluble zinc oxide has been used as skin ointment in topical applications to treat a variety of dermatological disorders. Treatment of surgical patients daily with oral doses of 50mg zinc (as Zinc sulphate) has been shown to enhance wound healing. Chronic ulcers have been healed successfully by the use of oral Zinc sulphate which led to the increase of zinc plasma concentration to between 30-45µmole/L.
Richest sources of dietary zinc include whole grains(germs),seeds, nuts, eggs and leafy vegetables, shellfish, dairy products. Zinc is not really stored and is readily lost from the body through faeces, sweating, urine, menstruation. During tissue metabolism and repair, the amount of zinc excreted is greatly increased.
Zinc plays essential role in DNA synthesis and cell division, a constituent of many dehydrogenase enzymes, erythrocyte carbonic anhydrase (essential for acid-base balance).anti-oxidant enzymes such as superoxide dismutase (SOD) which mops up free reactive oxygen species that are cell destructive. Zinc is involved in the binding of insulin within the beta cells of Islets of Langerhans, necessary for male reproductive functions and spermatogenesis especially in the production of testosterone by the Leydig cells. Collagen synthesis and degradation is facilitated by collaginase, a zinc-dependent enzyme.
Zinc deficiency can result in thymic atrophy. Studies have also revealed that symptoms of growth retardation, skin lesions and impaired sexual development was observed in adolescent malnourished boys in Iran and Egypt and was traced to their consumption of phytate bread. Acrodermatitis enteroparthica with symptoms of severe skin lesions, diarrhea ,loss of hair (alopedica) and mental disturbances result from zinc deficiency.
Research has shown that zinc plays a significant role in skin and connective tissue metabolism. The Greeks used Calamine solution on the skin to treat disorders. Zinc, usually in the form of insoluble zinc oxide has been used as skin ointment in topical applications to treat a variety of dermatological disorders. Treatment of surgical patients daily with oral doses of 50mg zinc (as Zinc sulphate) has been shown to enhance wound healing. Chronic ulcers have been healed successfully by the use of oral Zinc sulphate which led to the increase of zinc plasma concentration to between 30-45µmole/L.
BLOOD UREA NITROGEN AND CLINICAL CORRELATIONS
Urea is a by-product of amino acid catabolism which occurs in the liver. Urea is filtered by the glomerulus. The glomerular filtrate flows through the proximal tubule and urea is re-absorbed and returned to the blood stream. Blood urea levels are sensitive indicators of renal disease.
Elevated blood urea nitrogen (BUN) is termed Azotemia. Azotemia results from either protein catabolism or impaired kidney function. Elevated protein catabolism may result from the following; consumption of a high proteinous meal, upper gastro-intestinal tract bleeding in which case blood is being digested and absorbed. Azotemia can be pre-renal, renal and post-renal respectively.
Pre-renal azotemia results from underperfusion of the kidney and this is as a result of dehydration, mild glomerulonephritis, hemorrhagic shock and so on. These factors compromises renal blood flow with respect to tubular function. Urine sodium is normally low because the kidney responds to low blood flow by trying to retain all the sodium it can accommodate.
Renal azotemia usually results from acute tubular necrosis, chronic interstitial nephritis and chronic glomerulonephritis. Such patients may develop a disease condition called Isosthenuria.
Post-renal azotemia occurs as a result of obstruction of urinary flow as observed in prostate problems, kidney stones, tumours and carcinomas.
In acute renal failure, blood urea nitrogen increases around 20mg/dl each day.(Normal BUN is 8-25mg/dl or 2.9-8.9mmol).Decreased levels of blood urea nitrogen (BUN) may appear as a result of the following; lack of protein as seen in Celiac disease and in some patients with Nephrotic syndrome, severe liver disease such as cirrhosis, hepatitis, enzyme dysfunction and paracetamol toxicity.
Elevated blood urea nitrogen (BUN) is termed Azotemia. Azotemia results from either protein catabolism or impaired kidney function. Elevated protein catabolism may result from the following; consumption of a high proteinous meal, upper gastro-intestinal tract bleeding in which case blood is being digested and absorbed. Azotemia can be pre-renal, renal and post-renal respectively.
Pre-renal azotemia results from underperfusion of the kidney and this is as a result of dehydration, mild glomerulonephritis, hemorrhagic shock and so on. These factors compromises renal blood flow with respect to tubular function. Urine sodium is normally low because the kidney responds to low blood flow by trying to retain all the sodium it can accommodate.
Renal azotemia usually results from acute tubular necrosis, chronic interstitial nephritis and chronic glomerulonephritis. Such patients may develop a disease condition called Isosthenuria.
Post-renal azotemia occurs as a result of obstruction of urinary flow as observed in prostate problems, kidney stones, tumours and carcinomas.
In acute renal failure, blood urea nitrogen increases around 20mg/dl each day.(Normal BUN is 8-25mg/dl or 2.9-8.9mmol).Decreased levels of blood urea nitrogen (BUN) may appear as a result of the following; lack of protein as seen in Celiac disease and in some patients with Nephrotic syndrome, severe liver disease such as cirrhosis, hepatitis, enzyme dysfunction and paracetamol toxicity.
IRON-AN ESSENTIAL ELEMENT IN LIVING ORGANISMS
Iron is the most abundant trace element found in the human body. It is one of the transition elements. The total amount of iron in the body ranges from 2-6grammes. The mean amount found in both males and females is 50mg/kg and 40mg/kg respectively. Studies show that erythrocytes contain 70% iron, ferritin 24% iron, myoglobin 4% iron. Dietary iron is predominantly in the form of organic complexes but ferrous and ferric iron and elemental iron are also present. The reduction of ferric iron to ferrous iron is facilitated by the anti-oxidant action of vitamin C and by the sulphydryl groups of sulphur- containing amino acids. Hence, a diet containing plenty of vitamin C and protein enhances iron absorption.
Naturally chelated iron in the form of heme groups is present in meat and blood- containing tissues such as heart, liver, and kidney and is absorbed more readily than iron found in plants. Vegetarians are more likely to suffer iron deficiency since iron is less available in plants. Pumpkin leaves are a good source of iron. Brocoli has very good iron content and with probably little oxalate or phytate and so may be considered a good source of plant food iron. Eggs are low in iron because of the presence of phosvitin. Generally factors that inhibit calcium and magnesium absorption also inhibit iron absorption.
Iron deficiency is the most common cause of anaemia. Iron deficiency appears to be more common in pre-menopausal women who are subject to menstrual bleedings and pregnancies than in men. Symptoms include feeling of weakness and lascitude, paraesthesia, koilomychia, glossitis and stomatitis.
The definitive diagnostic signs are low red blood cell count, low haemoglobin concentration ,low mean corpuscular volume (MCV) and mean corpuscular heamoglobin concentration (MCHC). Treatment involves the following; by blood transfusion, giving iron supplements such as 250mg iron as ferrous sulphate (FeSo4) to adults, formulas supplemented with lactobionate can be given to infants and should be done with caution, and the consumption of ascorbate-containing fruits.
Iron toxicity should not be overlooked. Iron overload is a debilitating condition that results in the damage of the liver, heart, pancreas and so on. Two forms iron toxicity exists viz; genetic haemochromatosis and acquired haemochromatosis. Iron toxicity has been observed in children who consumed large quantities of iron-containing tablets. Treatment of iron toxicity is done via the following ways; inducing emesis to get rid of unabsorbed iron, the use of desferrioxamine-B a high affinity, iron chelating agent obtained from Streptomyces opilosus can provide relief.
Iron is an essential element need in life processes. However ,care should be taken so that iron deficiency do not result from poor nutrition and iron toxicity resulting from indiscriminate consumption.
Naturally chelated iron in the form of heme groups is present in meat and blood- containing tissues such as heart, liver, and kidney and is absorbed more readily than iron found in plants. Vegetarians are more likely to suffer iron deficiency since iron is less available in plants. Pumpkin leaves are a good source of iron. Brocoli has very good iron content and with probably little oxalate or phytate and so may be considered a good source of plant food iron. Eggs are low in iron because of the presence of phosvitin. Generally factors that inhibit calcium and magnesium absorption also inhibit iron absorption.
Iron deficiency is the most common cause of anaemia. Iron deficiency appears to be more common in pre-menopausal women who are subject to menstrual bleedings and pregnancies than in men. Symptoms include feeling of weakness and lascitude, paraesthesia, koilomychia, glossitis and stomatitis.
The definitive diagnostic signs are low red blood cell count, low haemoglobin concentration ,low mean corpuscular volume (MCV) and mean corpuscular heamoglobin concentration (MCHC). Treatment involves the following; by blood transfusion, giving iron supplements such as 250mg iron as ferrous sulphate (FeSo4) to adults, formulas supplemented with lactobionate can be given to infants and should be done with caution, and the consumption of ascorbate-containing fruits.
Iron toxicity should not be overlooked. Iron overload is a debilitating condition that results in the damage of the liver, heart, pancreas and so on. Two forms iron toxicity exists viz; genetic haemochromatosis and acquired haemochromatosis. Iron toxicity has been observed in children who consumed large quantities of iron-containing tablets. Treatment of iron toxicity is done via the following ways; inducing emesis to get rid of unabsorbed iron, the use of desferrioxamine-B a high affinity, iron chelating agent obtained from Streptomyces opilosus can provide relief.
Iron is an essential element need in life processes. However ,care should be taken so that iron deficiency do not result from poor nutrition and iron toxicity resulting from indiscriminate consumption.
HORMONES AND THEIR MEDICAL RELEVANCE
Hormones are chemical substances produced in the body or in a plant that encourages growth or influences how the cells and tissues function. Hormones act through specific high-affinity cellular receptors. Studies have shown that the locus of the interaction between hormone and receptor may be extracellular, cytosolic or nuclear depending on the hormone type. There is usually a change in membrane potential as a result of the opening or closing of a hormone-gated ion channel.
The mode of classification of hormones is as follows; endocrine hormones, paracrine hormones, and autocrine hormones. Endocrine hormones are released into the blood and carried to target tissues and cells throughout the body. Paracrine hormones are released into the extracellular space and diffuse into neighbouring target cells. Autocrine hormones are released by and affect the same cell, binding to receptors on the cell surface. Hormones can be grouped as follows; peptide hormones,catecholamine hormones and steroid hormones.
Peptide hormones are water-soluble and act extracellularly by binding to cell surface receptors that span the plasma membrane. They require the use of a second intracellular messenger such as cyclic AMP (cAMP).Examples include the pancreatic hormones insulin, glucagon and somastostatin,the parathyroid hormone and all the hormones of the hypothalamus and pitutiary. These hormones are concerned with carbohydrate metabolism and so on.
Catecholamines are produced in the brain and other neural tissues. They are water-soluble compounds and have tyrosine as their precursor. They function as neurotransmitters (e.g dopamine).The adrenal glands synthesize epinephrine and norepinephrine. They are released by exocytosis from their secretory vessicles. They also mediate a wide variety of physiological responses.
Steroid hormones are lipid-soluble. Their precursor is cholesterol. They travel to their target cells through the blood stream bound to carrier proteins. They are classified as glucocorticoids, mineralocorticoids, androgens and estrogen. Glucocorticoids (e.g cortisol) primarily affect carbohydrate metabolism, mineralocorticoids such as aldosterone regulate electrolyte concentrations in the blood. Androgens and estrogens are synthesized in the testes and ovaries. Testosterone and progesterone are sex hormones and affect sexual development and a variety or reproductive functions. Recent research indicates that they have more rapid effects, mediated by receptors localized in the plasma membrane.
Hormone replacement therapy is an invaluable tool used in the treatment of diseases. Insulin Dependent Diabetes Mellitus (IDDM) can be treated by beta cell replacement therapy, infertility can also be treated by carrying out a hormonal assay/profile on sex hormones found in humans to know their levels.
Hormones are invaluable chemical messengers whose roles are very vital in living organisms as they mediate metabolic and physiological processes.
The mode of classification of hormones is as follows; endocrine hormones, paracrine hormones, and autocrine hormones. Endocrine hormones are released into the blood and carried to target tissues and cells throughout the body. Paracrine hormones are released into the extracellular space and diffuse into neighbouring target cells. Autocrine hormones are released by and affect the same cell, binding to receptors on the cell surface. Hormones can be grouped as follows; peptide hormones,catecholamine hormones and steroid hormones.
Peptide hormones are water-soluble and act extracellularly by binding to cell surface receptors that span the plasma membrane. They require the use of a second intracellular messenger such as cyclic AMP (cAMP).Examples include the pancreatic hormones insulin, glucagon and somastostatin,the parathyroid hormone and all the hormones of the hypothalamus and pitutiary. These hormones are concerned with carbohydrate metabolism and so on.
Catecholamines are produced in the brain and other neural tissues. They are water-soluble compounds and have tyrosine as their precursor. They function as neurotransmitters (e.g dopamine).The adrenal glands synthesize epinephrine and norepinephrine. They are released by exocytosis from their secretory vessicles. They also mediate a wide variety of physiological responses.
Steroid hormones are lipid-soluble. Their precursor is cholesterol. They travel to their target cells through the blood stream bound to carrier proteins. They are classified as glucocorticoids, mineralocorticoids, androgens and estrogen. Glucocorticoids (e.g cortisol) primarily affect carbohydrate metabolism, mineralocorticoids such as aldosterone regulate electrolyte concentrations in the blood. Androgens and estrogens are synthesized in the testes and ovaries. Testosterone and progesterone are sex hormones and affect sexual development and a variety or reproductive functions. Recent research indicates that they have more rapid effects, mediated by receptors localized in the plasma membrane.
Hormone replacement therapy is an invaluable tool used in the treatment of diseases. Insulin Dependent Diabetes Mellitus (IDDM) can be treated by beta cell replacement therapy, infertility can also be treated by carrying out a hormonal assay/profile on sex hormones found in humans to know their levels.
Hormones are invaluable chemical messengers whose roles are very vital in living organisms as they mediate metabolic and physiological processes.
Saturday, November 14, 2009
ENZYME LINKED IMMUNOASSAY AND ITS MEDICAL RELEVANCE
Enzyme linked immunoassay commonly known as ELISA allows for rapid screening and quantification of the presence of an antigen in a sample. The principle guiding ELISA is as follows; a non-specific protein is used to wash a polystyrene plate inorder to block other proteins introduced in subsequent steps during the assay. The polystyrene is then treated with a solution which has the primary antibody. This is usually an antibody against the protein of interest. The unbound antibody is washed away and the surface is treated with a solution containing antibodies against the primary antibody.
These secondary antibodies have been linked to an enzyme that catalyses a reaction that forms a coloured product. The unbound secondary antibody is washed away, and the substrate of the antibody-linked enzyme is added.
Product formation (which is seen as colour intensity) is proportional to the concentration of the protein of interest in the sample.
Enzyme linked immunoassay is useful in the clinical laboratory for the diagnosis of Hepatitis B surface antigen, Human Immunodeficiency Virus and Herpes Simplex virus. Hepatitis is a liver disease that is associated with elevated levels of both direct (conjugated) and indirect plasma bilirubin. It is accompanied by jaundice. Human Immunodeficiency Virus results in Acquired Immune Defeciency Syndrome (AIDS).It results from opportunistic infections and ultimately results in death. Virologists and Immunologists are carrying out detailed research in the discovery of HIV vaccine, a cure to this global pandemic.
These secondary antibodies have been linked to an enzyme that catalyses a reaction that forms a coloured product. The unbound secondary antibody is washed away, and the substrate of the antibody-linked enzyme is added.
Product formation (which is seen as colour intensity) is proportional to the concentration of the protein of interest in the sample.
Enzyme linked immunoassay is useful in the clinical laboratory for the diagnosis of Hepatitis B surface antigen, Human Immunodeficiency Virus and Herpes Simplex virus. Hepatitis is a liver disease that is associated with elevated levels of both direct (conjugated) and indirect plasma bilirubin. It is accompanied by jaundice. Human Immunodeficiency Virus results in Acquired Immune Defeciency Syndrome (AIDS).It results from opportunistic infections and ultimately results in death. Virologists and Immunologists are carrying out detailed research in the discovery of HIV vaccine, a cure to this global pandemic.
PROTEINS-ESSENTIAL BUILDING BLOCKS OF LIFE
Proteins are macromolecules found in all living things. Proteins are naturally occurring polypeptides composed of monomers called amino acids. Proteins show great diversity such as enzymes, keratin, melanin and so on. The common feature associated with proteins irrespective of their structure is specificity. For instance, haemoglobin and myoglobin specifically binds molecular oxygen, enzymes bind to specific foreign bodies during immunological responses.
Proteins can either be simple or conjugated. Simple proteins are composed of amino acids while conjugated proteins contain other compounds apart from amino acids. Examples of simple proteins are glycine, histidine, phenylalanine, tyrosine and so on while conjugated proteins include glycoproteins and proteoglycans, lipoproteins. Glycoproteins and proteoglycans have carbohydrates as their prosthetic groups while lipoproteins have lipids as their prosthetic groups.
Proteins are known to fulfill diverse biochemical roles. It is also pertinent to note that functions of proteins are understood with respect to how the structure of such proteins allow the specific binding of particular molecules. The following are functions performed by proteins viz; enzymatic activity, transport and storage, mechanical functions, movement, protection and information processing.
Enzymes are known as biological catalysts and proteins.They are capable of enhancing rates of reactions by factors of about 1012. Haemoglobin and myoglobin are transport proteins. They are able to bind specifically to molecular oxygen. Haemoglobin makes oxygen to be readily available to tissues. Ferritin,is a protein that stores iron in various tissues.
Proteins perform structural functions. For instance, collagen provides tensile strength in skin, teeth and bone. Cell membranes and cell organelles are also partly composed of proteins. Movement via the use of muscles is enhanced by the interaction between protein filaments actin and myosin with myosin facilitating the enzymatic process that converts chemical energy of ATP into mechanical energy.
Antibodies and immunoglobulins are proteins found in mammals and they confer immunity by eliciting immunological responses. They also interact with complement to phagoticize and lyse foreign cells leading to their destruction. Signal transduction can be produced from hormones and light intensity detected by specific protein receptors which are capable of transfering the signal to the target cells via the process of biosignalling.For instance, in the biochemistry of vision, rhodopsin,a visual protein located in the retinal photoreceptors called rods and cones play an invaluable role in vision.
The role of proteins as building blocks in living organisms cannot be overemphasized. Hence, the need to consume proteinous foods should be encouraged.
Proteins can either be simple or conjugated. Simple proteins are composed of amino acids while conjugated proteins contain other compounds apart from amino acids. Examples of simple proteins are glycine, histidine, phenylalanine, tyrosine and so on while conjugated proteins include glycoproteins and proteoglycans, lipoproteins. Glycoproteins and proteoglycans have carbohydrates as their prosthetic groups while lipoproteins have lipids as their prosthetic groups.
Proteins are known to fulfill diverse biochemical roles. It is also pertinent to note that functions of proteins are understood with respect to how the structure of such proteins allow the specific binding of particular molecules. The following are functions performed by proteins viz; enzymatic activity, transport and storage, mechanical functions, movement, protection and information processing.
Enzymes are known as biological catalysts and proteins.They are capable of enhancing rates of reactions by factors of about 1012. Haemoglobin and myoglobin are transport proteins. They are able to bind specifically to molecular oxygen. Haemoglobin makes oxygen to be readily available to tissues. Ferritin,is a protein that stores iron in various tissues.
Proteins perform structural functions. For instance, collagen provides tensile strength in skin, teeth and bone. Cell membranes and cell organelles are also partly composed of proteins. Movement via the use of muscles is enhanced by the interaction between protein filaments actin and myosin with myosin facilitating the enzymatic process that converts chemical energy of ATP into mechanical energy.
Antibodies and immunoglobulins are proteins found in mammals and they confer immunity by eliciting immunological responses. They also interact with complement to phagoticize and lyse foreign cells leading to their destruction. Signal transduction can be produced from hormones and light intensity detected by specific protein receptors which are capable of transfering the signal to the target cells via the process of biosignalling.For instance, in the biochemistry of vision, rhodopsin,a visual protein located in the retinal photoreceptors called rods and cones play an invaluable role in vision.
The role of proteins as building blocks in living organisms cannot be overemphasized. Hence, the need to consume proteinous foods should be encouraged.
CANCER AND ITS TREATMENT
Cancer is a diseased growth in the body that often causes death. Cancer cells are referred to as oncogenes. Oncology is defined as the study of an abnormal mass of tissue or an abnormal cell population with a capacity for progressive growth. Persistence of growth is an important feature of cancerous or tumour cell that distinguishes them from other neoplastic cells. The neoplasm or new growth can either be benign (not dangerous) or malignant (harmful or dangerous).
Malignant tumours are divided into two groups viz; carcinomas and sarcomas. Carcinomas are composed of epithelial cells while sarcomas consist of connective tissues. Malignant cells prefer anaerobic glycolysis and produce more lactic acid than normal cells. Examples of cancers include lung cancer, breast cancer, cervical cancer and prostate cancer.
Two important concepts that are necessary for the treatment of cancers include growth fraction and cell cycle.Growth fraction has the following information; proportion of rapidly dividing neoplastic cells that effectively respond to chemotherapy, percentage of actively dividing cells in the cell cycle, an index of tumour enlargement. The cell cycle have various phases such as the synthesis phase (S-phase),mitosis phase (M-phase),gap phase represented by G1 and G2 respectively(here RNA synthesis ,protein synthesis and production of initiator proteins occur.),G0 represents the period when the cell go into a state of rest.
Cancer can be treated through the combination of three methods viz; surgery, radiotherapy and chemotherapy. Surgery involves the removal of malignant tumours from the affected part. For instance,lumpectomy involves the removal of malignant tumours from the breast. Radiotherapy employs the use of controlled radiation to treat malignant tumours. Effective chemotherapeutic approach to the treatment of cancer is based on the proper understanding of growth fraction and cell cycle concept. Growth fraction is an index of tumour enlargement and a higher growth fraction yields better results with chemotherapy.
Chemotherapeutic or anti-tumour drugs have the ability of affecting the various phases in the cell cycle. Antimetabolites are S-phase specific and examples include 5-fluorouracil,6-mecarptopurine,metotextrate and arabinosylcytosine. Vinca alkaloids are M-phase specific; two compounds are used which are vincaleucoblastine(VBL) and vincristine (VCR). Non-cell specific chemotherapeutic agents include alkylating agents such as nitrogen mustard, triethylenemelamine, and triethylene phosphorimide and antibiotics such as Actinomycin D, Adriamycin and so on.
It is also pertinent to note that anti-tumour drugs are associated with toxicity. Their therapeutic dose should be strictly obeyed. Examples of such effects include bone marrow depression, depletion of blood cells, loss of hair and so on.
The use Positron Emission Tomography (PET) scan is invaluable in the detection of cancerous growth in organs of the body.Conclusively,early detection of cancerous growth would ultimately enhance effective treatment of carcinomas and sarcomas occurring in humans.
Malignant tumours are divided into two groups viz; carcinomas and sarcomas. Carcinomas are composed of epithelial cells while sarcomas consist of connective tissues. Malignant cells prefer anaerobic glycolysis and produce more lactic acid than normal cells. Examples of cancers include lung cancer, breast cancer, cervical cancer and prostate cancer.
Two important concepts that are necessary for the treatment of cancers include growth fraction and cell cycle.Growth fraction has the following information; proportion of rapidly dividing neoplastic cells that effectively respond to chemotherapy, percentage of actively dividing cells in the cell cycle, an index of tumour enlargement. The cell cycle have various phases such as the synthesis phase (S-phase),mitosis phase (M-phase),gap phase represented by G1 and G2 respectively(here RNA synthesis ,protein synthesis and production of initiator proteins occur.),G0 represents the period when the cell go into a state of rest.
Cancer can be treated through the combination of three methods viz; surgery, radiotherapy and chemotherapy. Surgery involves the removal of malignant tumours from the affected part. For instance,lumpectomy involves the removal of malignant tumours from the breast. Radiotherapy employs the use of controlled radiation to treat malignant tumours. Effective chemotherapeutic approach to the treatment of cancer is based on the proper understanding of growth fraction and cell cycle concept. Growth fraction is an index of tumour enlargement and a higher growth fraction yields better results with chemotherapy.
Chemotherapeutic or anti-tumour drugs have the ability of affecting the various phases in the cell cycle. Antimetabolites are S-phase specific and examples include 5-fluorouracil,6-mecarptopurine,metotextrate and arabinosylcytosine. Vinca alkaloids are M-phase specific; two compounds are used which are vincaleucoblastine(VBL) and vincristine (VCR). Non-cell specific chemotherapeutic agents include alkylating agents such as nitrogen mustard, triethylenemelamine, and triethylene phosphorimide and antibiotics such as Actinomycin D, Adriamycin and so on.
It is also pertinent to note that anti-tumour drugs are associated with toxicity. Their therapeutic dose should be strictly obeyed. Examples of such effects include bone marrow depression, depletion of blood cells, loss of hair and so on.
The use Positron Emission Tomography (PET) scan is invaluable in the detection of cancerous growth in organs of the body.Conclusively,early detection of cancerous growth would ultimately enhance effective treatment of carcinomas and sarcomas occurring in humans.
AUTOIMMUNE DISEASES AND THEIR MEDICAL RELEVANCE
Autoimmune diseases results when tolerance to self antigens sometimes breaks down causing T or β cells or both to react against their own tissues. The response they produce contribute directly to the pathogenesis of the disease. Antibodies produced against tissue components may mediate cell or tissue destruction either alone or in conjunction with complement.
Myasthenia gravis is an autoimmune disease. Affected humans make antibodies against the acetycholine receptors on their own skeletal muscle cells. The antibodies intefer with the normal functioning of the receptors so that such patients become weak and can die since they cannot breathe.
Autoantibody to thyroglobulin leads to a disease called Hashiomoto’s thyroiditis. Systemic Lupus erythematosus is another autoimmune disease resulting from autoantibodies of nuclei, DNA,cytoplasmic soluble antigens.
ImmunoglobulinG (IgG) and immunoglobulin M (IgM) autoantibodies are associated with rheumatoid arthritis.Beta cells of the Islets of Langerhans in the pancreas are associated with Insulin Dependent Diabetes Mellitus(IDDM). Nephritis, Good pasteire’s syndrome have been linked to basement membrane autoantibodies. Parietal cells, intrinsic factor autoantibodies are associated with the disease pernicious anaemia.
Active chronic hepatitis results from smooth muscles microsomes autoantibodies.
Erythrocytes autoantibodies result in haemolytic anaemia. Primary biliary cirrhosis results from mitochrondria autoantibodies.
Chronic infection results from complement C3 autoantibodies.Complement component C3b enhances the ability of phagocytic cells such as microphages and neutrophils through their C3b receptors to bind,ingest and destroy the micro-organisms to which their C3b is bound.
Myasthenia gravis is an autoimmune disease. Affected humans make antibodies against the acetycholine receptors on their own skeletal muscle cells. The antibodies intefer with the normal functioning of the receptors so that such patients become weak and can die since they cannot breathe.
Autoantibody to thyroglobulin leads to a disease called Hashiomoto’s thyroiditis. Systemic Lupus erythematosus is another autoimmune disease resulting from autoantibodies of nuclei, DNA,cytoplasmic soluble antigens.
ImmunoglobulinG (IgG) and immunoglobulin M (IgM) autoantibodies are associated with rheumatoid arthritis.Beta cells of the Islets of Langerhans in the pancreas are associated with Insulin Dependent Diabetes Mellitus(IDDM). Nephritis, Good pasteire’s syndrome have been linked to basement membrane autoantibodies. Parietal cells, intrinsic factor autoantibodies are associated with the disease pernicious anaemia.
Active chronic hepatitis results from smooth muscles microsomes autoantibodies.
Erythrocytes autoantibodies result in haemolytic anaemia. Primary biliary cirrhosis results from mitochrondria autoantibodies.
Chronic infection results from complement C3 autoantibodies.Complement component C3b enhances the ability of phagocytic cells such as microphages and neutrophils through their C3b receptors to bind,ingest and destroy the micro-organisms to which their C3b is bound.
IMMUNOGLOBULINS AND THEIR RELEVANCE TO THE IMMUNE SYSTEM
Immunoglobulins are antibodies. These antibodies are glycoproteins.The antibodies which make up the immunoglobulins are found in heavy chains represented by the symbols γ,α,µ,and so on.Examples of immunoglobulins include immunoglobulin G (IgG),immunoglobulin A (IgA),immunoglobulin D(IgD) and immunoglobulin E (IgE).These immunoglobulins play vital roles in the immune systems of human and they are usually associated with diseases and immune responses.
Immunoglobulin G(IgG) represented by the symbol γ is a monomeric protein with molecular weight of 146,000 and sedimentation co-effiecient 7s.It is the most abundant of the immunoglobulins contributing between 70-75% of total plasma immunoglobulins.It is able to cross the placenta and activate the complement system.It provides antibody activity in tissues,contributes to immunity against many infectious agent that are blood-borne e.g. bacteria,viruses,parasites and some fungi.
Immunoglobulin M(IgM) represented by the symbol µ and accounts for about 10% of the total serum immunoglobulin.It is a pentameric protein with a molecular weight of 970,000.IgM are highly efficient against particulate antigens such as bacteria,they bind complement with high degree of efficiency.It is of greatest importance in primary immune response to interact with a foreign antigen that is introduced into a host.IgM is associated with rheumatoid arthritis.
Immunoglobulin A(IgA) represented by the symbol α and consist of between 15-20% of the total serum immunoglobulins in humans.IgA is the predominant immunoglobulin in sero-mucous secretions such as saliva,tracheobronchial secretion,colostrums milk and urinogenital secretions.It has a molecular weight of 385,000(i.e the secretory IgA existing mainly in the dimeric form).The secretory IgA is protected from proteolysis by the secretory component.
Immunoglobulin D(IgD) constitute less than 1% of the total plasma immunoglobulin but it is known to be present in large quantities on the membranes of circulatory B-lymphocyte.It plays a role in antigen triggered lymphocytes differentiation.(I.e neutrophils, eosinophils, monocytes, and basophils).
Immunoglobulin E(IgE) is present in trace amount in serum.It is found on the surface membrane of basophils and mast cells in all humans.It may play a role in active immunity to helminthic parasites but it is more commonly associated with immediate hyper-sensitivity diseases such as asthma,hay fever and eosinophilia.
Immunoglobulin G(IgG) represented by the symbol γ is a monomeric protein with molecular weight of 146,000 and sedimentation co-effiecient 7s.It is the most abundant of the immunoglobulins contributing between 70-75% of total plasma immunoglobulins.It is able to cross the placenta and activate the complement system.It provides antibody activity in tissues,contributes to immunity against many infectious agent that are blood-borne e.g. bacteria,viruses,parasites and some fungi.
Immunoglobulin M(IgM) represented by the symbol µ and accounts for about 10% of the total serum immunoglobulin.It is a pentameric protein with a molecular weight of 970,000.IgM are highly efficient against particulate antigens such as bacteria,they bind complement with high degree of efficiency.It is of greatest importance in primary immune response to interact with a foreign antigen that is introduced into a host.IgM is associated with rheumatoid arthritis.
Immunoglobulin A(IgA) represented by the symbol α and consist of between 15-20% of the total serum immunoglobulins in humans.IgA is the predominant immunoglobulin in sero-mucous secretions such as saliva,tracheobronchial secretion,colostrums milk and urinogenital secretions.It has a molecular weight of 385,000(i.e the secretory IgA existing mainly in the dimeric form).The secretory IgA is protected from proteolysis by the secretory component.
Immunoglobulin D(IgD) constitute less than 1% of the total plasma immunoglobulin but it is known to be present in large quantities on the membranes of circulatory B-lymphocyte.It plays a role in antigen triggered lymphocytes differentiation.(I.e neutrophils, eosinophils, monocytes, and basophils).
Immunoglobulin E(IgE) is present in trace amount in serum.It is found on the surface membrane of basophils and mast cells in all humans.It may play a role in active immunity to helminthic parasites but it is more commonly associated with immediate hyper-sensitivity diseases such as asthma,hay fever and eosinophilia.
PARKINSON’S DISEASE AND ITS TREATMENT
This is a disorder associated to dopamine oversecretion. Dopamie, a neurotransmitter
is involved in signal transduction in dopaminergic neurons. Basic symptoms include tremor, bradykinesia, reluctance to movement, and disturbed gait.
The cause of Parkinson’s disease is idiopathic.However,some clues were offered with the discovery of a selective dopamine toxicity produced by the synthetic compound 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP).MPTP was synthesized by illicit drug dealers in an attempt to produce MPPP, a synthetic heroin.When injected,MPTP produces neurological symptoms remarkably similar to Parkinson’s disease. The toxic effects of MPTP can be blocked by pargyline, an inhibitor of MAO-B which is normally distributed in serotonin containing neurons. Serotonin terminals are found in the substantia nigra.
The dopaminergic neurons of the substantia nigra project to the striatum,and their degeneration in Parkinson’s disease is associated with a reduction in the striated dopamine content. Parkinson’s disease has been linked to genetic disposition, viral infection, drugs such as resorpine deplete dopamine stores and doesnot inhibit the vessicularisation of dopamine stores. In the prevalence of Parkinson’s disease,1% of people of age 50years and above are affected. Beyond 25years,13% of such cells are lost per decade. β-N-methylaminoalanine,a plant product can also contribute to the incidence of Parkinson’s disease.
Treatment of Parkinson’s disease can be achieved via the use of the following; anticholinergic drugs, dopamine precursors, and dopamine receptor agonists such as bromocryptine. Parkinson’s disease has been treated successfully with the dopamine precursor 3,4-dihydroxyphenylalanine(L-DOPA),which unlike dopamine, is able to cross the blood-brain barrier. Inorder to prevent the rapid decarboxylation of L-DOPA in the bloodstream, decarboxylase inhibitors such as carbidopa are often given to increase the circulating levels of L-DOPA and decrease the side effects. Tolcapone is a selective inhibitor of catechol-o-methyltransferase is useful in the treatment of Parkinson’s disease. Catechol-o-methyltransferase converts L-DOPA to an inactive form, which contributes to the limited effects of L-DOPA treatment.
is involved in signal transduction in dopaminergic neurons. Basic symptoms include tremor, bradykinesia, reluctance to movement, and disturbed gait.
The cause of Parkinson’s disease is idiopathic.However,some clues were offered with the discovery of a selective dopamine toxicity produced by the synthetic compound 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP).MPTP was synthesized by illicit drug dealers in an attempt to produce MPPP, a synthetic heroin.When injected,MPTP produces neurological symptoms remarkably similar to Parkinson’s disease. The toxic effects of MPTP can be blocked by pargyline, an inhibitor of MAO-B which is normally distributed in serotonin containing neurons. Serotonin terminals are found in the substantia nigra.
The dopaminergic neurons of the substantia nigra project to the striatum,and their degeneration in Parkinson’s disease is associated with a reduction in the striated dopamine content. Parkinson’s disease has been linked to genetic disposition, viral infection, drugs such as resorpine deplete dopamine stores and doesnot inhibit the vessicularisation of dopamine stores. In the prevalence of Parkinson’s disease,1% of people of age 50years and above are affected. Beyond 25years,13% of such cells are lost per decade. β-N-methylaminoalanine,a plant product can also contribute to the incidence of Parkinson’s disease.
Treatment of Parkinson’s disease can be achieved via the use of the following; anticholinergic drugs, dopamine precursors, and dopamine receptor agonists such as bromocryptine. Parkinson’s disease has been treated successfully with the dopamine precursor 3,4-dihydroxyphenylalanine(L-DOPA),which unlike dopamine, is able to cross the blood-brain barrier. Inorder to prevent the rapid decarboxylation of L-DOPA in the bloodstream, decarboxylase inhibitors such as carbidopa are often given to increase the circulating levels of L-DOPA and decrease the side effects. Tolcapone is a selective inhibitor of catechol-o-methyltransferase is useful in the treatment of Parkinson’s disease. Catechol-o-methyltransferase converts L-DOPA to an inactive form, which contributes to the limited effects of L-DOPA treatment.
DIABETES MELLITUS AND TREATMENT
Diabetes mellitus is a devastating metabolic disease caused by insufficient insulin synthesis, increased insulin disruption or ineffective insulin action. The pancreas is the organ where the Islets of Langerhans is located. The beta cells found in the islets of Langerhans aid the production of insulin. Diabetes mellitus is classified into two groups viz; Insulin Dependent Diabetes Mellitus (IDDM).and Non-insulin Dependent Diabetes Mellitus (NIDDM).
Insulin Dependent Diabetes Mellitus (IDDM) is also referred to as Type 1 diabetes or Juvenile onset diabetes. It affects people below 30years or age. Inadequate amount of insulin is secreted because the beta cells of the pancreas have been destroyed. Three factors have been implicated in this destructive process of the beta cells viz; genetics, viral infections and autoimmunity (i.e the body’s immune system destroys insulin.)
Non-insulin Dependent Diabetes Mellitus (NIDDM) is also called Type2 or maturity (adult) onset diabetes.It affects people above 35years of age. This type of diabetes is caused by the insensitivity of target tissues it insulin.It occurs mostly in obese people.
Symptoms of diabetes mellitus include hyperglycemia (high blood glucose level) caused by inadequate cellular uptake of glucose, glucosuria (i.e glucose in urine).osmotic dieresis,dehydration may affect patients despite consumption of large volumes of fluids in very severe cases, polydipsia (excessive thirst) and polyphagia(excessive hunger).
When there is insufficient insulin to regulate glucose, three principal target tissues and organs (i.e. liver , adipose tissue ,and muscles) don’t absorb nutrients adequately. In severe cases of diabetes, despite increased appetite and food consumption, the failure to utilize glucose effectively results in body weight reduction.
The following methods can be used to treat both types of diabetes mellitus;diet(should include high content dietary fibres),through the use of insulin pump,beta cell replacement therapy ,pharmacotherapy(i.e sulphonyiureas ,biguanides),
alternative medicine(plant extracts).Research has shown that extracts from Loranthus bengwensis (African mistletoe) and Indian almond and several others possess hypoglycemic properties.
Diabetes mellitus is a devastating metabolic disease and should be given adequate medical attention so that it can be effectively managed and treated.
Insulin Dependent Diabetes Mellitus (IDDM) is also referred to as Type 1 diabetes or Juvenile onset diabetes. It affects people below 30years or age. Inadequate amount of insulin is secreted because the beta cells of the pancreas have been destroyed. Three factors have been implicated in this destructive process of the beta cells viz; genetics, viral infections and autoimmunity (i.e the body’s immune system destroys insulin.)
Non-insulin Dependent Diabetes Mellitus (NIDDM) is also called Type2 or maturity (adult) onset diabetes.It affects people above 35years of age. This type of diabetes is caused by the insensitivity of target tissues it insulin.It occurs mostly in obese people.
Symptoms of diabetes mellitus include hyperglycemia (high blood glucose level) caused by inadequate cellular uptake of glucose, glucosuria (i.e glucose in urine).osmotic dieresis,dehydration may affect patients despite consumption of large volumes of fluids in very severe cases, polydipsia (excessive thirst) and polyphagia(excessive hunger).
When there is insufficient insulin to regulate glucose, three principal target tissues and organs (i.e. liver , adipose tissue ,and muscles) don’t absorb nutrients adequately. In severe cases of diabetes, despite increased appetite and food consumption, the failure to utilize glucose effectively results in body weight reduction.
The following methods can be used to treat both types of diabetes mellitus;diet(should include high content dietary fibres),through the use of insulin pump,beta cell replacement therapy ,pharmacotherapy(i.e sulphonyiureas ,biguanides),
alternative medicine(plant extracts).Research has shown that extracts from Loranthus bengwensis (African mistletoe) and Indian almond and several others possess hypoglycemic properties.
Diabetes mellitus is a devastating metabolic disease and should be given adequate medical attention so that it can be effectively managed and treated.
DIAGNOSTIC ENZYMES AND THEIR CLINICAL IMPORTANCE
Enzymes are substances which catalyse metabolic and biochemical reactions. They are also known as biological catalysts. They enable metabolic and biochemical reactions to occur by lowering the activation energy of such reactions. The following are examples of diagnostic enzymes viz,lactatedehydrogenase(LDH),
creatinekinase(CPK),alkaline phosphatase,aspartate aminotransferace(AST),
alanine aminotransferace(ALT),acid phosphatase,glucose-6-phosphate dehydrogenase
and so on.
It is pertinent to note that the rationale for assaying enzyme activities is based on the premise that changes in activities reflect changes that have occurred in aspecific tissue or organ. Lactate dehydrogenase is an important enzyme involved in glucose metabolism.It is a tetramer(has 2 different subunits).It has five isoenzymes which are designated LDH1(HHHH),LDH2(HHHM),LDH3(HHMM),LDH4(HMMM) and LDH5(MMMM) respectively.Isoenzymes catalyse similar reaction but migrate differently when subjected to electrophoresis.Hence,lactate dehydrogenase activity is found in cardiac muscles and red blood cells( i.e LDH1,LDH2 and LDH4),skeletal muscle(LDH5),Liver (LDH5),kidney and brain (LDH3).Hence,increased LDH activities can be used to detect myocardial infarction,leukaemia,liver cirrhosis,tumours of the central nervous system.
Creatinekinase(CPK) exists as a dimeric enzyme with three isoenzymes CPK1,CPK2, and CPK3.The subunits are designated BB,MB, and MM respectively.Total creatinekinase activity shows an increase following myocardial infarction.It is pertinent to note that it is only when CPK2(i.e MB subunit) contribute more than 6% of the total creatinekinase activity that creatinekinase is implicated in myocardial infarction.
Alkaline phosphatase is an enzyme which transport phosphate groups across cell membranes of organs.It is found in the osteoblasts(bone cells),bile canali ( in the liver),small intestinal epithelium,proximal tubule(kidney) and placenta.Increase in alkaline phosphatase occurs mainly in bone diseases such as Paget disease,Osteogenic sarcoma,liver diseases and bilary tract.
Aspartate aminotransferase (AST) is an enzyme involved in transamination reactions. Transamination reactions produce keto and amino acids simultaneously in tissues where they occur.The assay of serum AST is particularly useful in the diagnosis of myocardial infarction.Elevated AST levels is indicative of damage to the myocardium. Although AST activity is still used in the diagnosis of myocardial infarction,it has been replaced to some extent by the assay of total creatinekinase activity(especially the isoenzyme CPK2).
Serum aminotransferase activities are sensitive indicators of parenchymal liver damage.Both alanine and aspartate aminotransferases have been implicated in infective hepatitis,infectious mononucleosis and hepatocellular damage.Exposure to toxic substances such as carbontetrachloride poisoning ,therapeutic substances such as chlormphenicol, cephalosporins and paracetamol overdose have also resulted in elevated AST and ALT activities.
The serum barely detectable glucose-6-phosphate dehydrogenase activity .An elevated activity is indicative of myocardial infarction .Red blood cells contain 120 – 240 units per 1012 cells. Defeciency of this enzyme can result in hemolytic anaemia through the use of antimalarials such as primaquine, aromatic compounds ,it has also been associated to Favism (resulting from Fava beans consumption).
Acid phosphatase is found in the prostate, red blood cells, small amounts are found in bone, liver, spleen and pancreas. The assay of serum acid phosphatase is mostly used to detect prostatic carcinoma and to monitor the treatment.
creatinekinase(CPK),alkaline phosphatase,aspartate aminotransferace(AST),
alanine aminotransferace(ALT),acid phosphatase,glucose-6-phosphate dehydrogenase
and so on.
It is pertinent to note that the rationale for assaying enzyme activities is based on the premise that changes in activities reflect changes that have occurred in aspecific tissue or organ. Lactate dehydrogenase is an important enzyme involved in glucose metabolism.It is a tetramer(has 2 different subunits).It has five isoenzymes which are designated LDH1(HHHH),LDH2(HHHM),LDH3(HHMM),LDH4(HMMM) and LDH5(MMMM) respectively.Isoenzymes catalyse similar reaction but migrate differently when subjected to electrophoresis.Hence,lactate dehydrogenase activity is found in cardiac muscles and red blood cells( i.e LDH1,LDH2 and LDH4),skeletal muscle(LDH5),Liver (LDH5),kidney and brain (LDH3).Hence,increased LDH activities can be used to detect myocardial infarction,leukaemia,liver cirrhosis,tumours of the central nervous system.
Creatinekinase(CPK) exists as a dimeric enzyme with three isoenzymes CPK1,CPK2, and CPK3.The subunits are designated BB,MB, and MM respectively.Total creatinekinase activity shows an increase following myocardial infarction.It is pertinent to note that it is only when CPK2(i.e MB subunit) contribute more than 6% of the total creatinekinase activity that creatinekinase is implicated in myocardial infarction.
Alkaline phosphatase is an enzyme which transport phosphate groups across cell membranes of organs.It is found in the osteoblasts(bone cells),bile canali ( in the liver),small intestinal epithelium,proximal tubule(kidney) and placenta.Increase in alkaline phosphatase occurs mainly in bone diseases such as Paget disease,Osteogenic sarcoma,liver diseases and bilary tract.
Aspartate aminotransferase (AST) is an enzyme involved in transamination reactions. Transamination reactions produce keto and amino acids simultaneously in tissues where they occur.The assay of serum AST is particularly useful in the diagnosis of myocardial infarction.Elevated AST levels is indicative of damage to the myocardium. Although AST activity is still used in the diagnosis of myocardial infarction,it has been replaced to some extent by the assay of total creatinekinase activity(especially the isoenzyme CPK2).
Serum aminotransferase activities are sensitive indicators of parenchymal liver damage.Both alanine and aspartate aminotransferases have been implicated in infective hepatitis,infectious mononucleosis and hepatocellular damage.Exposure to toxic substances such as carbontetrachloride poisoning ,therapeutic substances such as chlormphenicol, cephalosporins and paracetamol overdose have also resulted in elevated AST and ALT activities.
The serum barely detectable glucose-6-phosphate dehydrogenase activity .An elevated activity is indicative of myocardial infarction .Red blood cells contain 120 – 240 units per 1012 cells. Defeciency of this enzyme can result in hemolytic anaemia through the use of antimalarials such as primaquine, aromatic compounds ,it has also been associated to Favism (resulting from Fava beans consumption).
Acid phosphatase is found in the prostate, red blood cells, small amounts are found in bone, liver, spleen and pancreas. The assay of serum acid phosphatase is mostly used to detect prostatic carcinoma and to monitor the treatment.
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