Postnatal endocrine dysfunction induced by prenatal methylmercury or cadmium exposure in mice

The subtle and delayed effects of two heavy metals, cadmium and mercury, on the pituitary-adrenal axis of mice were examined. Exeprimental animals were exposed to the toxins both in utero and neonatally via treated mothers' milk. Plasma levels of corticosterone, adrenal production of corticosterone in vitro, and the capacity of the liver to metabolize corticosterone in vitro were studied in these animals as adults. Exposure to methylmercury resulted in diminished hepatic metabolism of corticosterone in vitro due to a loss of liver mass. Adrenal function and plasma levels of corticosterone were unaffected by treatment. Cadmium-exposed animals examined at 277 days of age showed no significant differences when compared to untreated controls. However, when studied at 460-480 days of age, a sex difference in the response to cadmium exposure was noted. In males, the major effect was enhancement of hepatic reductive capacity, while in females, adrenal secretory capacity was enhanced. Possible mechanisms of action and consequences of these effects are discussed.