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Impaired antioxidant status in diabetic rat liver. Effect of vanadate
A K Saxena1, P Srivastava, R K Kale
1Hormone and Drug Research Laboratory, School of Life Sciences, Jawaharlal Nehru University, New Delhi, India.
Abstract:
In vivo effects of vanadate on the antioxidant status of control and alloxan diabetic rats liver were examined. The increased oxidative stress during diabetes caused a decline in the activities of glutathione peroxidase (GPx), catalase (CAT), CuZn superoxide dismutase (CuZn-SOD) and Mn-superoxide dismutase (Mn-SOD) in the liver. Reduced glutathione (GSH) was also depleted, but the level of oxidized glutathione and glutathione reductase activity remained unchanged in the livers of diabetic rats. Vanadate treatment of diabetic rats (0.6 mg/mL in drinking water) resulted in almost complete restoration of GPx and Mn-SOD but caused only a partial restoration of CuZn-SOD. However, CAT and GSH were found to be lowered further in vanadate-treated diabetic rats as compared to untreated diabetic rat. Similar decreases in CAT and GSH levels were also observed in the vanadate-treated controls. These results suggest that vanadate, an insulin-mimetic agent, effectively normalized hyperglycemia, but unlike insulin, could not completely restore the altered endogenous defence mechanisms in diabetic liver.
Insights
Vanadate treatment normalized hyperglycemia in diabetic rats but did not fully restore liver antioxidant defenses. Key enzymes like catalase and glutathione levels were further reduced, unlike with insulin therapy.
Area of Science:
- Biochemistry
- Pharmacology
- Toxicology
Background:
- Diabetes mellitus is characterized by increased oxidative stress.
- Alloxan-induced diabetes in rats mimics human diabetic conditions.
- Antioxidant defense mechanisms are compromised in diabetic livers.
Purpose of the Study:
- To investigate the in vivo effects of vanadate on liver antioxidant status in diabetic rats.
- To compare vanadate's impact on antioxidant enzymes and glutathione levels with insulin's known effects.
Main Methods:
- Alloxan was used to induce diabetes in rats.
- Vanadate was administered in drinking water (0.6 mg/mL).
- Liver antioxidant status was assessed by measuring enzyme activities (GPx, CAT, CuZn-SOD, Mn-SOD) and glutathione levels (GSH).
Main Results:
- Diabetes significantly reduced GPx, CAT, CuZn-SOD, and Mn-SOD activities, and depleted GSH levels.
- Vanadate treatment restored GPx and Mn-SOD but only partially restored CuZn-SOD.
- Vanadate further decreased CAT and GSH in diabetic rats and also in control rats.
Conclusions:
- Vanadate effectively normalizes hyperglycemia in diabetic rats.
- Unlike insulin, vanadate does not fully restore altered antioxidant defense mechanisms in the diabetic liver.
- Vanadate administration can negatively impact endogenous antioxidant systems, even in non-diabetic individuals.