In utero exposure to methylmercury and Se deficiency converge on the neurobehavioral outcome in mice.

Pregnant female ICR mice, maintained on torula-based diets containing various amounts of Se (0.02, 0.05, or 0.4 mg/kg diet), were given methyl-mercury (MeHg; 0, 5, or 9 mg Hg/kg in total) on the 12-14th days of gestation. The neurobehavioral function of the offspring born to these dams was evaluated with respect to reflex and motor development, thermal preference, and open-field activity. Se deficiency per se as well as exposure to MeHg exerted additive or synergistic effects on the neurobehavioral functions examined. The group of mice most affected was the group given the lowest amount of Se and the highest dose of MeHg. Thus, the neurobehavioral outcome of in utero MeHg exposure and Se deficiency converged. Although the dietary level of Se did not affect the Hg concentration in the fetal brain, the Se concentration and the activity of glutathione peroxidase, a selenoenzyme, were severely depressed by MeHg in the neural tissue. The possibility that functional Se deficiency by MeHg exposure partly accounts for the neurobehavioral toxicity of MeHg is discussed.