Effect of vitamin E on blood glucose, insulin, lipid peroxides, and antioxidant system of streptozotocin-induced diabetes in rats

There is growing evidence that excess generation of highly reactive free radicals, largely due to hyperglycemia, causes oxidative stress which further exacerbates the development and progression of diabetes and its complications. There are multiple sources of oxidative stress in diabetes including non-enzymatic, enzymatic, and mitochondrial pathways. Vitamin E is a fat-soluble vitamin that prevents lipid peroxidation. The present study was carried out to test the effect of vitamin E on blood glucose, insulin, and lipid peroxides in blood and liver tissue of rats in relation to oxidative damage associated with diabetes induced by streptozotocin [STZ]. 24 male albino rats were randomly assigned to control [group I], streptozotocin [STZ]-induced diabetic rats [group II], the third group [vitamin E group] were STZ-induced diabetic rats fed 400 mg of vitamin E/kg diet. After 4 weeks of the induction of diabetes, rats were sacrificed and the following determinations were done on the blood, serum or plasma. Blood glucose, serum insulin, lipid peroxide concentration in plasma as malonyldialdehyde [MDA] level in nmol/g protein, the amount of thiobarbituricp acid reactive materials in plasma [TBARM], serum antioxidant capacity [assayed by measuring the total peroxy radical trapping capacity [TRAP] of serum, and serum superoxide dismutase, enzyme activity [SOD]. In the liver, the following parameters were determined: liver MDA, SOD and Glutathione peroxidase [GSH-Px] enzyme activaties, and Glutathione [GSH] concentration. Hyperglycemia, hypoinsulinemia were regarded in group II which were ameliorated by vitamin E administration. Oxidant stress was found in diabetic rats group II manifested by increase concentration of MDA-plasma and liver, increase TBARM concentration, and TRAP-plasma and serum respectively. Also increased serum SOD, liver SOD, and GSH-Px enzyme activities in these diabetic rats. Administration of vitamin E in the diet decreased the oxidant stress parameters [MDA, TBARM, and TRAP], increased the antioxidant defense parameter [increased GSH concentration in liver], and decreased the oxidant stress as manifested by the decrease in serum SOD enzyme activity; liver SOD; and GSH-Px enzyme activities. Vitamin E was found to be excellent for strengthening the antioxidant defense system in STZ-diabetic rats and it may therefore has a therapeutic role in combating the damaging effect of ROS in diabetes and preventing its complications

protective role of the angiotensin-converting enzyme inhibitor enalapril against gamma radiation induced organ toxicity in the rat

The present study was designed to evaluate the radioprotective efficacy of the angiotensin-converting enzyme inhibitor enalapril and the possible mechanisms of this radioprotection. This included the ability of prophylactic enalapril treatment to prevent or retard gamma radiation-induced organ toxicity and to protect tissue' antioxidant enzymes in the rat. Prior to irradiation rats were randomized to groups receiving enalapril or no treatment, in addition to a control group of non-irradiated, non-treated rats. Enalapril was administered intraperitoneally [0.1 mg/ kg body weight / day], 4 weeks before and 12 weeks after irradiation. Both groups were exposed to a single dose of 7GY gamma radiation. Irradiation induced significant elevations in the levels of blood urea nitrogen and serum creatinine and serum activities of lactate dehydrogenase [LDH], creatine kinase [CK], alanine amino transferase [ALT] and aspartate amino transferase [AST] compared to control values, indicative of renal, cardiac and hepatic injury. Also there was an increase in the serum levels of triglycerides, total cholessterol and LDL-cholesterol. On the contrary, HDL-cholesterol level was decreased. The heart, kidney and liver antioxidant enzymes including total glutathione peroxidase [total-GPX], glutathione reductase [GR] and superoxide dismutase [SOD] activities were inhibited, while malondialdehyde [MDA] level in these organs was elevated, indicative of increased lipid peroxidation. These data confirm the role of oxidative stress in radiation-induced organ toxicity and points to the possible antioxidative mechanisms of the radioprotective action of enalapril, which might be mediated by improving the balance between reactive oxygen species and antioxidant enzymes. Moreover, the beneficial effect of enalapril on serum lipid profile is suggested to be an additional mechanism of radioprotection