استخدام فيتامين C كمضاد للأكسدة للتقليل من أثار التصلب العصيدي المستحدث تجريبيا ببيرو كسيد الهيدروجين في الأرانب

Abstract EN

This study was designed to investigate the effect of vitamin C in alleviating the changes in lipid profile and the atherosclerotic lesions induced experimentally by (0.5 %) H2O2 in drinking water.

Twenty four adult males rabbits were divided randomly into four equal (a control and 3 treated "T") groups for 19 weeks : 1-The Control group: Which was given normal drinking water.

2-Group (T1) : was given 0.5 % H 2O2 in drinking water.

3-Group (T2) : which was handled as T1, in addition to vitamin C (100 mg / kg / day) along the experiment.

4-Group (T3) : was treated as T1 till the atherosclerotic lesions were established at the week 13, then the animals received 100 mg / kg of vitamin C daily for 6 weeks.

Blood samples were taken at the weeks 5, 13, 16 and 19 of the experimental period to measure the levels of total cholesterol (TC), triglycerid (TG), HDL-C, LDL-C and VLDL-C in plasma.

Samples of aortic tissue were taken to study the histopatholpgical changes.

The results showed that H2O2 caused an increase in TC, TG, LDL, VLDL-C and a decrease in HDL-C concentration in plasma.

The histopathological sections showed lesions of atherosclerosis in the aorta as fatty streaks and foam cells.

Moreover, results showed that treatment with vitamin C caused a dereased in the VLDL-C, LDLC, TG and TC levels and an increase in the HDL-C concentration in plasma.

and regression of atherosclerotic lesions.

Results of the present study suggest that the oxidative stress (produced by 0.5 % H2O2) has an important role in pathogenesis of atherosclerosis in the rabbits and vitamin C has an important effect in reducing and preventing some of the oxidative stress changes in lipid profile and atherosclerotic lesions of the aorta.

It is worthed to report that this is the first study undertaken in using vitamin C as an antioxidant to minimize the oxidative stress effects of H2O2 in rabbits as a model for atherosclerosis in mammals.