Attenuation of mitochondrial oxidative stress by morin during chemical carcinogen-mediated mammary carcinogenesis

In this study we evaluated the effects of morin on the mitochondrial functions with reference to mitochondrial citric acid cycle enzymes, respiratory chain complex enzymes, membrane bound ATPases and protein-bound carbohydrates in mammary tissues of 7,12-dimethyl benz(a)-anthracene (DMBA)-induced mammary carcinoma of Sprague-Dawley rats. Adult female Sprague-Dawley rats were induced mammary carcinoma by administration of DMBA (25 mg/kg b.wt.) orally. The normal and cancer-induced rats were treated with morin (50 mg/kg b.wt.) for three times per week for 13 weeks. Cancer-induced rats showed a significantly increased level of lipid peroxidation (LPO) products and protein-bound carbohydrates with concomitant decreased levels of nonenzymic antioxidants (vitamin C, reduced glutathione [GSH]) and vitamin E and enzymic antioxidants (superoxide dismutase [SOD]), catalase (CAT) and glutathione peroxidase (GPx) in the mammary tissue. Decreased levels of ATPases, citric acid cycle enzymes and respiratory chain enzymes were observed in the mammary tissue of tumor bearing group of rats. Treatment with morin brought back lipid peroxidation products, nonenzymic and enzymic antioxidants to near normalcy. Since morin treatment decreases lipid peroxidation and enhances antioxidants and enzymes involved in the biochemical pathways, it may play a critical role in oxidative stress-related changes in cancer-induced rats and may possess a potent antioxidant potential to protect subcellular organelles being damaged by oxidative stress.