Exposure of neonatal mice to an estrogenic endocrine disruptor, bisphenol A, resulted in a malfunction of the testes when the animals became adults. The effect of bisphenol A was cancelled out by concurrent administration of retinol acetate, a naturally occurring metabolite of vitamin A. In contrast, the effect of endocrine disruption became more severe in mice neonatally exposed to bisphenol A and nursed by mothers fed a vitamin A-deficient diet only a few days before and after parturition. These results clearly show that maternal vitamin A is important for relieving in a baby the effect of endocrine disruption caused by environmental xenoestrogens, and suggest that the changes in the content of vitamin A and similar physiological factors in the habitat may be worth considering in studies on environmental disruptors.