Abstract
Malathion-induced teratisms in the chick embryo included hind limb, beak, and feather defects as well as overall growth retardation. Various metabolites were injected along with malathion into fertile eggs in an attempt to determine the possible effect of the latter compound on metabolism. Of those compounds injected tryptophan prevented both the malformations and the growth retardation while nicotinamide, nicotinic acid, and quinolinic acid prevented the malformations only. Other compounds related to tryptophan by electronic reactivity enhanced the effect of malathion. A cholinesterase assay on embryo homogenates revealed no relationship between cholinesterase levels and teratisms.
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