Журнал лекарственного метаболизма и токсикологии
Открытый доступ
ISSN: 2157-7609
ISSN: 2157-7609
Ashima Pathak, Abhishek S Rathore, Vimal Bhutani and R Pathak
Background: Diabetes is the third leading cause of death in the United States after heart disease and cancer. It is a chronic and progressive illness that causes considerable morbidity and premature mortality. Research shows that zinc, an essential trace element responsible for over 300 enzyme functions, can aid in normalizing the negative effects of diabetes mellitus. Zinc plays an important role in major metabolic pathways, and also regulates insulin production by pancreatic tissue and glucose utilization by muscle and fat cells. But not many studies have been performed regarding the antioxidative role of zinc on brain during diabetes.
Methods: Male Wistar rats were given zinc in the form of ZnSO4 .6H2 O at a dose level of 227 mg/L daily in their drinking water and diabetes was induced by giving a single intraperitoneal injection of alloxan (150 mg/kg body weight).
Results: The present study indicated that during diabetes, lipid peroxidation in brain was found to be increased while levels of GSH and the activity of catalase and SOD were found to be decreased. Zinc, however, was able to decrease lipid peroxidation and increase catalase activity in brain, but it further decreased the activity of GR and SOD.
Conclusion: Our findings suggest that oxidative stress occurs in diabetic state and that the oxidative damage to tissues may be a contributory factor in complications associated with diabetes. Zinc seems to positively influence lipid peroxidation and oxidative stress, but whether this effect is mediated by Cu, Zn- SOD needs to be explored further.