Critical time periods and the effect of tryptophan in malathion-induced developmental defects in Xenopus embryos

Xenopus laevis embryos were exposed to the organophosphorus insecticide malathion or its metabolite malaoxon during the first four days of development. The compounds produced the following defects in a dose dependent manner: reduced size, abnormal pigmentation, abnormal gut, enlargement of the atria and aorta, bent notochord and lowered NAD+ levels. Notochords were bent downward between the third and sixth somites with concurrent compression of the somites. Anterior intestine diameter was increased with a concurrent reduction in the number of intestinal loops. When tryptophan was administered along with malathion, NAD+ was measured at control levels or above, yet neither severity nor incidence of defects were reduced. The reduction of NAD+ does not seem to be responsible for the defects seen in Xenopus as occurs for some defects in avian species. In experiments to determine critical time of exposure, the final 48 h, which follow organogenesis and are primarily devoted to growth and development, seem most critical.