Kabay Sibel Canbaz, Ozden Hilmi, Guven Gul, Ustuner M Cengiz, Degirmenci Irfan, Olgun Esra Gurlek, Unal Nedim
Department of Neurology, Osmangazi University, Eskisehir, Turkey.
Clin Invest Med. 2009 Oct 1;32(5):E314-21. doi: 10.25011/cim.v32i5.6918.
To evaluate the histopathological and antioxidant effects of vitamin E (VE) treatment on brain tissue in streptozotocin (STZ)-induced diabetic rats.
Thirty two male Wistar albino rats were used. The study comprised four groups of 8 rats: Group A - untreated group, group B - diabetic group, group C - VE and group D - diabetic plus VE. In the diabetic groups, diabetes was induced by a single intraperitoneal injection of 65 mg/kg STZ. Vitamin E was given 50 mg/kg/day i.p. for three weeks. Concentrations of glucose, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were detected in the haemolysate.
Glucose concentrations were increased in the blood of the STZ-treated rats compared with those in the diabetic groups (group B and D). The MDA concentrations in the brain from diabetic rats increased, whereas the GPx, SOD, CAT concentrations decreased. Treatment with VE returned concentrations of MDA, GPx, SOD and CAT toward control values. The MDA concentration in the diabetic group (20.65+/-2.24 nmol/mg Hb) was decreased compared with the VE treated group (15.54+/-1.32 nmol/mg Hb). There were no pathological differences between untreated and VE treated rats' brains. Neuronal ischemic damages were determined in STZ-induced diabetic rats. Ischemic neuronal alterations in group B (diabetic) had more damage than group D (diabetic + VE).
The study revealed neuroprotective effects of VE on ischemic damage in diabetic central neuronal cells, caused by diabetic oxidative stress.
