Abstract
Exposure of silkworm larvae to sub-lethal doses of organophosphorus insecticides such as parathion and disulfoton, induced specific ovicidal action on their subsequent eggs. The embryos of eggs laid developed to the stage just before or just after hatching and then died. Although embryonic respiration and cholinesterase activity of affected eggs were almost normal, approximately 2 days before anticipated hatching, abnormalities appeared. About 2.7 ng parathion (4.8 ppm/egg weight) or about 3.6 ng disulfoton (6.6 ppm/egg weight) were transferred from the maternal body to the egg, this is equal to the lethal dose for hatched larva. Based on our results we suggest that some of the chemical agent entered the female body during the larval stage, became residual due to the absence of neutralization or excretion, was transferred to the egg during egg formation, and subsequently inhibited the embryonic cholinesterase activity, resulting in death just prior to hatching or death just after hatching.