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Biomedical subjects

N Sekar

Publications and source records attributed to N Sekar.

11 recordsLinked to original sources
PubMed1991

Antitumor effect of echitamine chloride on methylcholonthrene induced fibrosarcoma in rats.

Echitamine chloride a plant alkaloid from Alstonia scholaris has been used to examine the anticancer effects on methylcholanthrene-induced fibrosarcoma. Echitamine chloride dissolved in saline (10 mg/kg body weight) and injected subcutaneously for 20 days in fibrosarcoma rats has exhibited significant regression in tumor growth. The altered activities of plasma and liver transaminases and gamma-glutamyl transpeptidase and lipid peroxidation in fibrosarcoma have been corrected to near normal after echitamine chloride treatment. The decreased liver glutathione content and the lowered activities of glutathione peroxidase, superoxide dismutase and catalase have also been reversed to near normals after echitamine chloride treatment.

Alkaloids↗
PubMed1991

Insulin mimetic role of vanadate on plasma membrane insulin-receptors.

Vanadate possesses insulin-mimetic effects, and has been reported to correct the metabolic imbalances in streptozotocin-induced diabetes. Rats were made diabetic by a single i.v. injection of streptozotocin (55 mg/kg body weight) in citrate buffer. After the onset of diabetes, the diabetic rats were treated with sodium orthovanadate (0.3 mg/ml) for 15 days. The increased percentage of 125 I insulin binding to the liver plasma membrane insulin receptors and increased plasma membrane phospholipids were found to be reduced significantly in vanadate treated diabetes. Hence the mode of action of vanadate may be similar to that insulin.

Animals↗
PubMed1991

Effects of vanadate on plasma lipoprotein profiles in experimental diabetic rats.

The insulin-like effects of vanadate have been intensively studied in the biological system. Lipids and lipoprotein profiles are altered in diabetes. Rats were made diabetic by a single i.v. injection of streptozotocin (55 mg/kg body weight) in citrate buffer. After the overt of diabetes, the diabetic rats were treated with sodium orthovanadate (0.3 mg/ml) for fifteen days. The altered cholesterol, phospholipids and triglycerides in plasma lipoprotein fractions (HDL, LDL and VLDL) were found to be reverted back to near normal levels in vanadate treated diabetic rats.

Animals↗
PubMed1991

Toxic effect of morphine and the antagonistic role of naloxone on isolated rat hepatocytes.

Isolated rat hepatocytes when incubated with various concentrations of morphine exhibited a marked decrease in the level of glutathione and resulted in cell death. The formation of electrophilic intermediates make the cell more susceptible to peroxidative attack, which is reflected by the increase in thiobarbituric acid reactant material as well as lipid fluorescence. Pretreatment of cells with naloxone blocked the morphine induced damage and itself has no cytotoxic effects on the cells.

Animals↗
PubMedDate not supplied

Antioxidant effect of vanadate on experimental diabetic rats.

The activities of enzymes involved in cellular defence mechanisms such as superoxide dismutase, catalase, glutathione peroxidase and glutathione level have been found to be altered in experimental diabetes. Rats were made diabetic by a single i.v. injection of streptozotocin (55 mg/kg body weight) in citrate buffer. After the onset of diabetes, the diabetic rats were treated with sodium orthovanadate (0.3 mg/ml) for 15 days. Decreased activities of glutathione peroxidase, catalase, superoxide dismutase and glutathione content found in diabetic rats were corrected to near normal. The altered levels of plasma lipid peroxide, glycoproteins and erythrocyte membrane phospholipids in diabetic rats were restored to control levels by vanadate treatment. These observations clearly indicate the antioxidant potential of vanadate on experimental diabetes.

Animals↗
PubMedDate not supplied

Insulinic actions of vanadate in diabetic rats.

Oral administration of sodium orthovanadate (0.3 mg/dl) normalizes blood glucose and reduces glycosylated HbA1 levels in streptozotocin induced diabetic rats without any increase in the serum insulin levels. However, diabetic condition reappears after withdrawal of vanadate. Assays of carbohydrate metabolizing enzymes clearly indicate that vanadate activates the glycolysis, glycogenesis and depresses the glycogenolysis and gluconeogenesis in diabetic rats. These results demonstrate that vanadate substitutes insulin action in chronic experimental diabetics.

Animals↗