Abstract

Pregnant rats were given a single subcutaneous injection of methylmercuric chloride (at 4 or 8 mg/kg) on the ninth day of gestation. Foetal (2 days prenatal), newborn and postnatal (6 days post partum) animals from the methylmercury-treated mothers were investigated with respect to parameters of carbohydrate metabolism. In the absence of any physical abnormalities, foetal rats exposed to methylmercury in utero showed diminished concentrations of plasma glucose and liver glycogen concentrations and a lower hepatic glucose-6-phosphatase activity compared to control animals. Newborn rats from the methylmercury-treated mothers showed an impairment in glycogen mobilization in the first hours of extra-uterine life which was accompanied by a severe and protracted hypoglycaemic response. Postnatal rats exposed to methylmercury in utero exhibited higher liver glycogen concentration and decreased body weights compared to control rats. The results point to a derangement of perinatal carbohydrate metabolism in the offspring of pregnant rats exposed briefly to low doses of methylmercury during gestation (“metabolic teratogenesis”). The postnatal hypoglycaemic episode in exposed rats may contribute to the pathogenesis of the neurological disturbances revealed by these animals in later life.

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