Effect of quercetin on galactose-induced hyperglycaemic oxidative stress in hepatic and neuronal tissues of Wistar rats.

In recent times there has been great demand for natural products that have possible preventive action against diabetes and its secondary complications. Keeping this in mind, this study was undertaken to investigate the influence of the flavonoid, quercetin, on oxidative stress markers and the antioxidant defence system of hepatic and neuronal tissues from galactose-induced hyperglycaemic rats. Weanling male Wistar rats were treated with 30% galactose in AIN 93 diet (group B, n=8) to induce hyperglycaemia. Control rats received normal Stock AIN 93 diet (group A, n=8). The third set of rats received group B diet with quercetin at 400 mg/100 g diet (group C, n=8). Glucose levels and body weights were measured on a weekly basis for four weeks to monitor the hyperglycaemia induced by galactose feeding. Parameters involved in the pathogenesis of galactose-induced hyperglycaemia, which included organosomatic index, protein content, antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), tryptophan fluorescence, content of protein carbonyls, prooxidant malonaldehyde (MDA) and glutathione (GSH) in hepatic and neuronal tissues were determined at the end of the fourth week. The study suggest that quercetin counters the pro-oxidant effects of galactose-induced hyperglycaemic stress, as there was a significant reversal of changes with respect to body weights, organosomatic index of hepatic and neuronal tissues, lipid peroxidation, protein carbonyl content, reduced glutathione and activities of antioxidant enzymes. In addition, treatment with quercetin appears to reduce the osmotic stress induced by hyperglycaemia, as assessed by polyol pathway enzyme aldose reductase. These results imply that inclusion of quercetin in the diet controls, to some extent, galactose-induced hyperglycaemia and its attendant complications.