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Biomedical subjects

R Selvam

Publications and source records attributed to R Selvam.

At least 55 records · Page 3Linked to original sources
PubMed1991

Induction of oxalate binding by lipid peroxidation in rat kidney mitochondria.

Enhanced oxalate binding (150-180% of control) was observed in kidney, liver, brain and heart, after subjecting them to lipid peroxidation in presence of iron. Kidney mitochondrial oxalate binding was stimulated by different promoters, and the order of stimulation was Fe2+ greater than t-BH greater than ascorbic acid greater than Fe3+ greater than H2O2. Oxalate binding was maximum when iron concentration was between 1-2 mM. The iron-induced oxalate binding was inhibited by reduced glutathione, beta-mercaptoethanol, alpha-tocopherol and hydroxyl ion scavengers, histidine and mannitol. Catalase inhibited both Fe(2+)-H2O2 induced oxalate binding and lipid peroxidation reactions, suggesting that the induced oxalate binding in mitochondria was mediated through the hydroxyl radical reaction mechanism.

Animals↗
PubMed1991

Effect of radical treatment on erythrocyte lipid peroxidation in Plasmodium vivax-infected malaria patients.

Elevated levels of thiobarbituric acid reactive substances and increased in vitro Heinz body formation in erythrocytes of Plasmodium vivax-infected malarial patients were observed. Radical treatment with chloroquine and primaquine increased the per cent maximal release of thiobarbituric acid reactive substances. Antioxidant enzymes, superoxide dismutase and catalase were decreased significantly in vivax malaria. Superoxide dismutase showed restoration of enzyme activity while catalase activity was increased significantly following therapy, suggesting an active involvement of free radical mechanism.

Animals↗
PubMed1991

The haematology of Plasmodium vivax before and after chloroquine and primaquine treatment in north Madras area.

Changes in haematological parameters were studied in 35 Plasmodium vivax infected patients and compared with those in an equal number of normal subjects. Patients showed a high proportion of schizonts of P. vivax (1-2%). Hb, PCV and RBC values were significantly decreased (p less than 0.001) with increasing parasitaemia. Osmotic fragility was slightly increased (15%) when compared to controls and ranged from 0.385-0.405 (50% hypo-osmotic haemolysis given at gm/dl of NaCl) with increasing parasitaemia in the patients. Decreased levels of lymphocyte and increased levels of eosinophils and monocytes were seen in P. vivax infected patients. However, after treatment with chloroquine and primaquine, all the haematological parameters were restored to near normal levels.

Blood Cell Count↗
PubMed1991

Glucose-6-phosphate dehydrogenase deficiency and malaria--a study on north Madras population.

Blood samples from 381 healthy individuals and 236 malaria patients residing in North Madras were studied for glucose-6-phosphate dehydrogenase deficiency. The incidence of this deficiency in this area was found to be 10.05%. Partially deficient healthy females showed a protective trend against malarial infection with the Chi-squared test approaching statistical significance.

Female↗
PubMed1991

Increased plasma lipidperoxidation in vitamin B-6 deficient rats.

Lipidperoxidation in plasma of rats fed with vitamin B-6 deficient diet for a period of 12 weeks was studied with pair-fed controls. Plasma pyridoxal 5'-phosphate, alanine amino transferase and aspartate amino transferase, the markers of vitamin B-6 status, were significantly low in vitamin B-6 deficient rats. Plasma malondialdehyde level, conjugated dienes and lipofuscin like pigments were increased in vitamin B-6 deficiency. Increased levels of plasma lipids, calcium, iron and copper were observed in vitamin B-6 deficiency. Plasma susceptibility to lipidperoxidation was maximal in vitamin B-6 deficiency, upon stimulation by the promotors, Fe2+, Fe3+, Cu2+, ascorbate, t-butyl hydroperoxide and hydrogen peroxide.

Animals↗
PubMed1991

Effect of oral methionine and vitamin E on blood lipid peroxidation in vitamin B6 deficient rats.

Lipid peroxidation in blood of vitamin B6 deficient rats was significantly increased when compared to pair-fed controls. The observed increased lipid peroxidation in vitamin B6 deficiency was correlated with high levels of lipids, metal ions and low levels of antioxidants, alpha-tocopherol, ascorbic acid and reduced GSH. Supplementation of methionine or vitamin E along with the vitamin B6 deficient diet restored the levels of antioxidants to near normal and also protected against oxidative stress. However plasma TBARS level as well as total lipids were still elevated in M-B6 diet fed rats and normalized in E-B6-d rats.

Animals↗
PubMed1990

Effect of oral methionine on blood lipid peroxidation and antioxidants in alloxan-induced diabetic rats.

Supplementation of thiol compounds has been suggested to protect against the toxic effects of reduced oxygen species by contributing to the thiol pool of the cell. The present study was designed to determine whether supplementation of methionine in the diet of diabetic animals protected against the oxidative stress in diabetic pathology. Oral methionine was administered at a dosage of 330 mg/100 g feed to diabetic rats. The effect was compared with the effect of insulin administration. Levels of lipid peroxides were measured in plasma, erythrocytes, and erythrocyte membrane. Anti-oxidants were measured in plasma. Diabetic condition was associated with increased lipid peroxidation and depletion in antioxidant levels. Although methionine did not affect the level of blood glucose and some of the antioxidants, it lowered the lipid peroxide content in blood. Erythrocyte lipid peroxidation activity was unaffected by methionine treatment. Administration of insulin lowered both plasma and erythrocyte lipid peroxide levels.

Journal Article↗
PubMed1990

Increased lipid peroxidation in kidney of vitamin B-6 deficient rats.

Lipid peroxidation in kidney of rats fed with vitamin B-6 deficient diet for a period of 12 weeks was studied with pair-fed controls. The basal lipid peroxide level as well as the degree of susceptibility to lipid peroxidation in presence of promotors such as NADPH, ascorbate, t-butyl hydroperoxide, Fe2+, Cu2+ and oxalate, were increased in vitamin B-6 deficient kidney. The observed increased lipid peroxidation in vitamin B-6 deficient kidney was correlated with high levels of lipids, copper, iron, calcium and oxalate, low levels of antioxidants and antioxidant enzymes and increased levels of hydroperoxides and hydroxyl radicals.

Animals↗
PubMed1989

Induction of lipid peroxidation in calcium oxalate stone formation.

The function of lipid peroxidation and the anti-peroxidative enzymes of rat liver and kidney were investigated under hyperoxaluric and stone forming conditions. The experimental animals showed higher malondialdehyde content in liver and kidney than that of control. A significant increase in malondialdehyde release was observed in the experimental liver or kidney when incubated with either ferrous sulphate or hydrogen peroxide compared to that of control liver or kidney. Superoxide dismutase activity was not affected in the hyperoxaluric rats while there was a moderate increase in the stone forming rats when compared to control. Highly significant decrease in catalase activity was observed in both conditions in liver and kidney compared to control.

Animals↗
PubMed1989

Lipids changes in rat tissues in experimental urolithiasis.

Total lipids, free and ester cholesterol, triglyceride and phospholipids were determined in plasma, liver, kidney and intestine in control and calculi producing diet (CPD) fed rats. Cholesterol, phospholipids and triglycerides were increased in plasma while they were decreased in all the three tissues of CPD fed rats, compared to that of control. Distribution studies of phospholipids in the tissues of treated rats showed marked decrease in the concentration of the major lipids, i.e., PC, PE, PI and SPH. However, significant increase in absolute concentration as well as percent distribution of phosphatidic acid in kidney of treated rats was observed.

Animals↗
PubMed1989

Increased lipid peroxidation in the erythrocytes of kidney stone formers.

The level of lipid peroxidation was significantly increased in erythrocytes and erythrocyte membrane in patients with stone disease. Increased activities of catalase and acetylcholinesterase in the erythrocyte membrane were observed, while hemolysate displayed no significant change in superoxide dismutase activity. The amount of phospholipids in the RBC membrane of patients was significantly increased. Peroxidation was stimulated by oxalate in vitro and was further enhanced in the presence of ferrous ion. The changes in lipid peroxidation and antioxidant enzymes are suggestive of chemical alteration of the RBC membrane during urolithiasis.

Acetylcholinesterase↗
PubMed1986

Binding of oxalate to mitochondrial inner membranes of rat and human kidney.

Oxalate bound specifically to homogenates of rat kidney and liver but not to homogenates prepared from heart, lung, skeletal muscle, spleen, stomach, small or large intestine. In the renal cortex, binding was localized to the inner mitochondrial membrane where it was enriched fourfold when compared to homogenate. Binding of the oxalate reached equilibrium in two minutes at 23C. Analysis of the binding sites by Scatchard plot indicated that the maximum binding capacity was 49 pmol./mg. protein and the apparent dissociation constant (Kd) was 43 nM. The IC50 of oxalate was 0.25 microM. Among the inhibitors studied the IC50 was in the following order: oxalate less than oxamate less than parabanate less than glyoxalate less than oxaloacetate less than malate less than citrate = glycollate. Heat and treatment with lubrol abolished the binding completely. Binding was not enhanced by the presence of calcium in the incubation medium; neither was it inhibited by the presence of calcium together with its transport inhibitors. A binding substance with some characteristics similar to the rat mitochondrial binding factor was also found in the human renal cortex.

Animals↗
PubMed1982

Determination of glucocerebroside, sphingomyelin, free fatty acid and total lipid by thin-layer chromatography and charring-scintillation quenching.

A previously described method has been extended to various specific lipids of liver and brain. The basic method involves thin-layer chromatography followed by charring to reveal the bands. The intensity of each band is determined by suspending the silica gel in a radioactive scintillation gel and measuring the optically quenched activities. The lipids are extracted with hexane/isopropanol and, in the case of total lipid determinations, the extract is simply applied to a silica gel plate and charred without use of a development step. For brain cerebroside, the extract is applied to the plate and developed in the usual way. For liver cerebroside, the dried lipid extract is fractionated with a silica gel column to purify the glycolipid, which is then purified further by development with a plate. For sphingomyelin the ester type lipids in the extract are cleaved by alkali for 1 min and the resultant lipids are applied directly to the thin-layer plate. Free fatty acids are chromatographed and measured after a preliminary solvent partitioning to remove most lipids. The method is useful for samples of 5-40 micrograms. Methods for quantitative application of samples to plates are described. A modification of the Camag sample streaker is described which yields precise 1-cm streaks.

Animals↗