Inhibition of halothane-induced lipid peroxidation by misoprostol without hepatoprotection.

In mice, the synthetic prostaglandin derivative misoprostol failed to protect against liver damage induced by acetaminophen, carbon terachloride,1,1-dichloroethylene or thioacetamide. In rats, misoprostol (20-100 micrograms/kg p.o.) markedly reduced early increments of plasma enzyme activities (glutamate-pyruvate-transaminase, GPT; sorbitol dehydrogenase, SDH) in a model of halothane-induced liver injury; the most effective dose in this respect (20 micrograms/kg) significantly depressed halothane-induced ethane exhalation indicating in vivo lipid peroxidation. Repeated treatment with misoprostol (20 micrograms/kg p.o.) still diminished halothane-induced elevations of enzyme activities over 48 h, but failed to prove hepatoprotection by histomorphological examinations. It is concluded that the antiperoxidative properties of misoprostol are not paralleled by an hepatoprotection, which was indicated by significant reductions of liver-specific plasma enzyme activities, but not confirmed by the morphological picture.