ZINC, IRON, AND PEROXIDATION IN LIVER-TISSUE - CUMULATIVE EFFECTS OF ALCOHOL-CONSUMPTION AND VIRUS-MEDIATED DAMAGE - A PRELIMINARY-REPORT

In an attempt to elucidate further the mechanisms involved in alcohol- mediated liver damage and the correlation between alcohol and viruses in chronic liver lesions, we determined the levels of liver glutathion e (GSH), thiobarbituric acid reactive substances (TBARS), iron (Fe), a nd zinc (Zn) in 31 patients with chronic viral hepatitis (CAH), 6 with alcohol-related chronic hepatitis (CALD), 6 with alcoholic cirrhosis (AC), 8 with primary biliary cirrhosis (PBC), and 10 healthy controls (C). Liver GSH was significantly lower in CALD and AC patients (p < 0. 005). TBARS levels were significantly higher in CAH, CALD, and PBC pat ients (p < 0.001, < 0.02, and < 0.001, respectively). In CAH patients, alcohol consumption correlated inversely with GSH and directly with T BARS (p < 0.05). Patients with both CAH and alcohol abuse had a furthe r reduction in Liver GSH levels (p < 0.005). Tissue levels of Fe were significantly increased in CALD and AC patients with respect to contro ls and CAH patients, whereas no significant difference was observed in Zn. These data confirm that patients with chronic ethanol exposure re veal a depletion in liver GSH content clearly correlated with an incre ase in lipid peroxidation and Fe liver storage. On the other hand, the se findings appear to suggest no significant change in Zn levels in ch ronic hepatitis.