Modification of Methylmercury Toxicity by Selenium in the Developing Nervous System

摘要

Golden hamsters (Mesocricetus auratus) were used in the study. Pregnant females were injected intraperitoneally (IP) daily with 2.0 mg/kg body weight of methylmercuric chloride and/or sodium selenide on gestational days 10-15. Control animals were injected similarly with equal volumes of saline solution. The transplacental transfer of mercury, the number and size of the pups, the average brain weights of the pups, neuronal migration, and neuropathology in the cerebellum of the pups were analyzed. It was found that methylmercury crossed the placenta readily and accumulated in the fetus, particularly in the fetal brain. Electron microscopy revealed various degenerative changes in the nerve cells, particularly involving the dendritic processes of the neurons. Such neuronal damage appeared to be permanent and still could be found in animals six months after birth. In sum, methylmercury was found to cross the placental barrier very readily and had a detrimental effect on the developing nervous system. Selenium, although not completely eliminating the neurotoxic effects of methylmercury, appeared to reduce the pathological impact on the nervous system.