Zinc, iron, and peroxidation in liver tissue. Cumulative effects of alcohol consumption and virus-mediated damage--a preliminary report.

Abstract

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 glutathione (GSH), thiobarbituric acid reactive substances (TBARS), iron (Fe), and 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 patients (p < 0.001, < 0.02, and < 0.001, respectively). In CAH patients, alcohol consumption correlated inversely with GSH and directly with TBARS (p < 0.05). Patients with both CAH and alcohol abuse had a further reduction in liver GSH levels (p < 0.005). Tissue levels of Fe were significantly increased in CALD and AC patients with respect to controls and CAH patients, whereas no significant difference was observed in Zn. These data confirm that patients with chronic ethanol exposure reveal a depletion in liver GSH content clearly correlated with an increase in lipid peroxidation and Fe liver storage. On the other hand, these findings appear to suggest no significant change in Zn levels in chronic hepatitis.