Abstract
The weak carcinogen N-methyl-N'nitro-N-nitrosoguanidine injected 1 h before the potent carcinogen β-propiolactone decreased by half the incidence of induction and the number of tumors of the rumen in SWR mice. β-Propiolactone decreased the incidence of lung adenomas induced by weak carcinogen in these mice. Mutual effects of both compounds, which are inactivated in the body by a nonenzymatic route and requiring no metabolic activation for realization of their carcinogenic effects are probably realized through competition for targets.
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