Reproductive and developmental toxicity of triphenyltin chloride in rats.

ABSTRACT Reproductive and developmental toxicity of triphenyltin chloride (TPTCI) was evaluated in rats. Although no significant increase in the incidence of fetuses with malformations was observed following administration of TPTCI during organogenesis, a significant increase in the incidence of postimplantation embryonic loss was found. TPTCI during early pregnancy, especially on days 0–3 of pregnancy, caused implantation failure, i. e., preimplantation embryonic loss. The effects of TPTCI on the uterine function, as a cause of implantation failure, were determined using pseudopregnant rats. TPTCI was given on days 0–3 of pseudopregnancy and the decidual cell response was induced on day 4 of pseudopregnancy. Rats was sacrificed on day 9 of pseudopregnancy and the uterine weight served as an index of the uterine decidualization. A significantly lower weight of the uterus, which indicates the suppression of uterine decidualization, was found at the doses which induced implantation failure. These doses of TPTCI also caused a significant decrease in the progesterone levels, which indicates reduced ovarian function. These findings suggest that TPTCI exerts adverse effects on uterine decidualization correlated with the reduction in serum progesterone levels and these effects are responsible, at least in part, for the implantation failure induced by TPTCI.