Publication

Abstract : Alcohol consumption and health outcomes are complex and multidimensional. Ethanol (1.6g / kg body weight/ day) exposure initially affects liver function followed by renal function of 16–18 week-old male albino rats of Wistar strain weighing 200–220 g. Chronic ethanol ingestion increased in thiobarbituric acid reactive substances level and glutathione s-transferase activity; while decreased reduced gluatathione content and activities of catalase, glutathione peroxidase and glutathione reductase in a time dependent manner in the hemolysate. Though superoxide dismutase activity increased initially might be due to adaptive response, but decreased later. Elevation of serum nitrite level and transforming growth factor-b1 activity indicated that long-term ethanol consumption may cause hepatic fibrosis and can elicit pro-angiogenic factors. However, no alteration in vascular endothelial growth factor-C activity indicated that ethanol consumption is not associated with lymphangiogenesis. Therefore, we conclude that long-term ethanol-induced toxicity is linked to an oxidative stress, which may aggravate to fibrosis and elevate pro-angiogenic factors, but not associated with lymphangiogenesis.