[Protective effect of vitamin E on diabetes induced apoptosis and oxidative stress in rat heart tissue]

The purpose of this study was to determine and to assess the protective effect of vitamin E on cardiomyocyte apoptosis and oxidative stress status in the heart under hyperglycemic conditions, in vivo. Wistar male rats [n=16] at 6 months of age were made hyperglycemic by STZ. Same age, normal wistar rats [n=8] were used for comparison [controls]. Diabetic rats were divided into two groups, the nontreated and those treated with vitamin E [300mg/kg/daily]. Diabetic rats exhibited severe apoptosis in cardiomyocytes. Also significant increases in lipid peroxidation as measured by 8- isoprostan, protein oxidation as measured by protein carbonyl content and superoxide dismutase were observed after 6 weeks. Catalase activity was shown to increase in controls compared to nontreated rats. A distinct elevation in the HbA1C, QT interval and a decline in the activity of catalase were also observed. Vitamin E treated rats shown significant decline in apoptosis, lipid peroxidation, protein carbonyl and QT interval compared to nontreated rats. Vitamin E decreased the incidence of apoptosis in cardiomyocytes, lipid peroxidation and improve antioxidant enzyme in the diabetic hearts of rats. Further research to confirm the findings is recommended

[Measurement of renal vitamin e for assessment of iron and nitric oxide interaction in rats]

Oxidative stress has been implicated as an important factor in induction of many disorders such as nephropathy and cancer. Iron by producing hydroxyl radical can cause this kind of stress. On the other hand nitric oxide [n0] when its concentration is high results in oxidative stress. Iron and NO have some interactions in each other function but there is no total agreement on this. For example in one study NO prevents and in another it worsens iron toxicity. The study aims at evaluating the interaction between NO and iron on renal oxidative stress. Renal vitamin E level was measured as an index of oxidative stress. Sixty-four male rats were divided into eight 8- rat groups as follows: I-SHAM [normal saline], 2- Fe [iron dextran], 3- ARG [L-arginine precursor of NO synthesis], 4- Fe+ARG, 5- L-NAME [Blocker of NO production], 6- Fe+L-NAME, 7- DFO [Defleroxamine, shelator of iron], and 8- ARG+DFO. All injections were performed intraperitoneally. Twenty hours after injections, right kidneys were removed and their concentration of- vitamin E was measured by high performance liquid chromatography. The results showed that in group Fe there was a reduction in vitamin E compared to group SHAM [P<0.05]. In-group Fe+L-NAME there was a further reduction in vitamin E compared to group SHAM [P<0.01]. There was no significant difference between group SHAM with Fe+ARG. Group Fe+L-NAME also showed a significant decrease in vitamin E compared to group Fe+ARG [P<0.05]. We conclude that NO can prevent iron induced oxidative stress and can act as an antioxidant