Abstract

OXIDATIVE STRESS IN ALCOHOLIC CIRRHOSIS

Sameer R Kulkarni*, K. Pratibha Ravindra and C.Y.Dhume.

Abstract

Alcoholism can lead to various medical complications, like perturbed alcohol metabolism, liver cirrhosis and hormonal changes associated with pancreatitis, osteoporosis, immune impairment and impaired fertility. Most of the toxic and metabolic disorders that results from long-term ethanol abuse can be explained on the basis of the metabolism of ethanol by alcohol dehydrogenase (ADH) and the associated generation of reduced NADH or by the Microsomal ethanol-oxidizing system (MEOS), with the induction of Cytochrome P-4502E1 and other Microsomal enzymes, as well as by the toxic effects of acetaldehyde produced by both pathways, primarily in the liver. Studies have shown that ethanol consumption may result in increased oxidative stress with increased formation of lipid peroxides and free radicals. However, very few reports are avaliable on their involvement in the toxicity of alcoholic cirrhosis. The present study was conducted to evaluate some of the components of antioxidant defense system and oxidative damage in 80 male patients of alcoholic cirrhosis. The results were compared with 70 healthy non alcoholic male volunteers. Patients were subjected to detailed clinical examination and laboratory investigations. Blood samples were collected for estimating Malondialdehyde (MDA), Superoxide dismutase (SOD), Catalase (CAT), Reduced Glutathione (GSH), Glutathione peroxidase (GPx) and Glutathione Reductase (GR). However, the core utility of MDA was found to be significantly (p

Keywords: Alcohol cirrhosis, Antioxidant enzymes, Lipid peroxidation.