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Abstract

Effect of 2-Hydroxy-4-methoxy Benzoic Acid Isolated from Hemidesmus indicus on Erythrocyte Membrane Bound Enzymes and Antioxidant Status in Streptozotocin-induced Diabetic Rats

Author(s): M Gayathri, K Kannabiran

In the present study, the effect of 2-hydroxy-4-methoxy benzoic acid isolated from roots of Hemisdesmus indicus on the erythrocyte membrane bound enzymes and antioxidant status in streptozotocin-induced diabetic rats was investigated. The streptozotocin-induced diabetic rats were treated with 2-hydroxy-4-methoxy benzoic acid (500 μg/kg/day) for 7 weeks by oral intubation and compared with glibenclamide, a standard hypoglycemic agent (100 mg/kg). The erythrocyte membrane was isolated and the activity of Na+/K+-dependent ATPases, Ca2+-ATPases, Mg2+-ATPases were determined. Superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, vitamins C, vitamin E, plasma reduced glutathione and erythrocyte glutathione, reduced glutathione content in the tissues was also assayed. Administration of 2-hydroxy-4-methoxy benzoic acid to diabetic rats significantly (F>0.05 and P<0.001) elevated the activity of total ATPases, Na+/K+ ATPase, Mg2+ ATPase and Ca2+ ATPase to near normal level. The activities of catalase, superoxide dismutase and glutathione peroxidase and glutathione-S-transferase in erythrocytes were decreased significantly (F>0.05; P<0.001) in diabetic rats. Diabetic rats treated with 2-hydroxy-4-methoxy benzoic acid showed a significant (F>0.05; <0.001) increase in the enzymic antioxidants in erythrocytes. The elevated levels of vitamin E and low level of vitamin C and glutathione level in plasma and erythrocytes were observed in diabetic rats when compared to control rats and were restored significantly (F>0.05; P<0.001) after the administration of 2-hydroxy-4-methoxy benzoic acid. This study concludes administration of 2-hydroxy-4-methoxy benzoic acid supports the restoration of antioxidant defence, reduces the free radial production, lipid peroxidation and the glycosylation of haemoglobin in diabetic rats.

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