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We investigated sex difference in the influence of dietary protein deficiency on the fate of methylmercury (MeHg) using both sexes of C57BL/6N mice and Wistar rats to determine the universality of the influence. One day after oral administration of MeHg (20 mol/kg), regardless of sex and species, urinary Hg excretion was suppressed by dietary protein deficiency, whereas fecal excretion was not affected. At that time, tissue Hg concentrations in both sexes of the specified species were similarly influenced by dietary protein deficiency except for the gonads, although the influence on Hg concentration in each tissue was different between species. Regardless of sex, dietary protein deficiency resulted in the following alterations: in mice, the brain Hg concentration increased but the concentrations in the liver, kidney, blood and plasma were not affected, and in rats, Hg concentrations in the liver and blood increased but the renal concentration decreased with similar concentrations in the plasma and brain. Hg concentration in the testes was enhanced in mice but suppressed in rats by dietary protein deficiency, whereas that in the ovary was not affected in either species, suggesting that Hg accumulation in the gonads would be more changeable in males than in females by dietary protein deficiency. These results suggest that, regardless of sex, dietary protein deficiency similarly influences the fate of MeHg, except for the gonads. It is also suggested that a decrease in urinary excretion of MeHg by dietary protein deficiency might be universal.

This paper describes the deficits in brain regional growth of rats treated with methylmercury (MeHg) among the postnatal developing phases. Rats were orally administered 10 mg/kg/day of methylmercury chloride (MMC) for 10 consecutive days from postnatal days 1 (PD-1), -14 and -35, which corresponded to the early-, late-and postbrain growth spurt, respectively. Weight-matched control rats were periodically isolated from their mother or diet and placed in an incubator for intervals of 4 to 10 hr in order to adjust the body weight to MMC-treated rats. The earlier the postnatal phase the higher the resistance to body weight loss induced by MMC. The rats were dissected on the day after final MMC treatment and the weight of organs and their mercury (Hg) concentrations were measured. Hg accumulation in the brain on the day after final treatment with 10 mg/kg/day of MMC was highest in the rats treated during the late-brain growth spurt. On the other hand, Hg accumulations in the liver and kidney increased rapidly with development of postnatal phases. Then, the brain/kidney and brain/liver ratio of Hg concentration were much higher in early postnatal rats than in later one. The weight of brain regions in MMC-treated rats was compared with those in weight-matched control rats. The significantly lower weight of the cerebrum, cerebellum and midbrain + diencephalon were confirmed in rats treated with MMC during the early-brain growth spurt. The significantly lower cerebellum weight was confirmed in rats treated with MMC during the late-brain growth spurt. The Significant differences were not observed in the brain regions in rats treated during post-brain growth spurt. In the case of human, a similar reduction of the brain weight occurred in the fetal and non-fetal infantile Minamata disease patients. The experiment using postnatal rats succeeded to reproduce the deficit in the brain growth during the earlyand late brain growth spurt by MMC treatment.

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