Antidotal effects of dimethyl sulphoxide against paracetamol-, bromobenzene-, and thioacetamide-induced hepatotoxicity

Abstract

In mice the hepatotoxic effects of paracetamol (0·5–1·0 g kg−1, orally) as evidenced by increased serum enzyme activities of the aminotransferases and sorbitol dehydrogenase were dose-dependently inhibited by simultaneous treatment with dimethyl sulphoxide (DMSO 0·25–1·0 g kg−1, i.p.). DMSO was also active against bromobenzene- and thioacetamide-induced hepatotoxicity, but failed to protect mice against carbon tetrachloride-induced liver damage. Hepatic glutathione depletion in mice amounting to 94% after paracetamol (0·5 g kg−1, orally) and to 60% after bromobenzene (0·25 ml kg−1, orally) was dose-dependently reduced by the simultaneous administration of DMSO (0·25–1·0 g kg−1, i.p.). This indicates less conjugation of the toxic metabolites of paracetamol and bromobenzene to liver glutathione (G-SH) in the presence of DMSO.