Mitochondrial damage, cytotoxicity and apoptosis in iron-potentiated alcoholic liver fibrosis: amelioration by taurine.

Taurine effectively prevents ischemia-induced apoptosis in the cardiomyocytes and hypothalamic nuclei. The present study explores the influence of taurine on mitochondrial damage, oxidative stress and apoptosis in experimental liver fibrosis. Male albino Wistar rats were divided into six groups and maintained for a period of 60 days as follows: Group I, control; Group II, ethanol treatment [6 g/(kg/day)]; Group III, fibrosis induced by ethanol and iron (0.5% w/w); Group IV, ethanol + iron + taurine (2% w/v); Group V, ethanol + taurine treatment and Group VI, control + taurine treatment. Hepatocytes isolated from ethanol plus iron-treated rats showed decreased cell viability and redox ratio, increased reactive oxygen species formation, lipid peroxidation, DNA fragmentation, and formation of apoptotic bodies. Liver mitochondria showed increased susceptibility to swell, diminished activities of mitochondrial respiratory chain complexes and antioxidants. Taurine administration to fibrotic rats restored mitochondrial function, reduced reactive oxygen species formation, prevented DNA damage, and apoptosis. Thus taurine might contribute to the amelioration of the disease process.