Vinyl acetate, a structural analog of vinyl carbamate, fails to induce enzyme-altered foci in rat liver.

The development of hepatic enzyme-altered foci (ATPase, GGTase) was investigated after dosing vinyl acetate (200 and 400 mg/kg per day, orally) to newborn rats for 3 weeks, with or without subsequent promotion by phenobarbital. Whereas the structurally related compounds vinyl carbamate and vinyl chloride induce enzyme-altered foci under comparable experimental conditions, no foci were observed in vinyl acetate-treated animals at the age of 14 weeks. This is consistent with investigations on metabolism and pharmacokinetics of vinyl acetate which show that this compound, after entering the organism, is immediately split by blood esterases and thus may not be available for epoxidation to an ultimately carcinogenic metabolite.