Protective effect of N-acetylcysteine on reduced glutathione, reduced glutathione-related enzymes and lipid peroxidation in methanol intoxication.

The primary metabolic appropriation of methanol is oxidation to formaldehyde and then to formate. These processes are accompanied by formation of superoxide anion and hydrogen peroxide. This paper reports data on the effect of N-acetylcysteine (NAC) on reduced glutathione (GSH) and on activity of some GSH-metabolising enzymes in the liver, erythrocytes and serum of rats intoxicated with methanol (3 g/kg b.w.) during 7 days after intoxication. Methanol administration, increasing concentration of the lipid peroxidation products, decreased the liver glutathione-peroxidase and glutathione reductase (GSSG-R) activities, GSH concentration and total antioxidant status (TAS). The use of NAC after methanol ingestion apparently diminished lipid peroxidation, elevated the GSH level in the liver and erythrocytes, and increased activity of GSH-related enzymes in the serum, erythrocytes and in the liver. These results suggest that NAC exerts its protective effect by acting as a precursor for glutathione, the main low molecular antioxidant and as a free radical scavenger.