Protective effects of selenium against methylmercury neurotoxicity: a morphological and biochemical study

The protective effect of selenium (as sodium selenite) against methylmercury neurotoxicity was investigated morphologically and biochemically. Young adult Charles River rats were divided into 4 groups and were treated (i. p. injection) with methylmercury chloride (2 mg MeHg/kg b.w.), sodium selenite (2 mg Se/kg b.w.), both MeHg and Se, or with saline solution for 8 weeks. Four animals from each group were randomly selected for pathological investigation. These animals were sacrificed by intracardiac perfusion. The dorsal root ganglia (DRG) were dissected out for both light and electron microscopic examination. Six animals from each group were injected with 14 C-leucine 3 hours prior to sacrifice. The brains (cerebrum and cerebellum) of these animals were removed, weighed, homogenized and subjected to liquid scintillation analysis. Morphological investigation revealed extensive degenerations of the dorsal root fibers and destructions of neuronal Nissl substances in animals treated with MeHg alone. In MeHg/Se-treated animals, no neuronal change was observed and the nerve fiber damage was also significantly reduced. Proliferative thickenings of the myelin membrane, however, were observed in some dorsal root fibers. These proliferative membrane thickenings tend to protrude into the axonal compartment of the nerve fibers causing compression and shrinkage of the axons. It is believed that this proliferative, membraneous whirling phenomenon may represent a simultaneous destruction/repair condition of the myelin sheaths. Biochemical investigation also demonstrated a significant suppression of amino acid uptake (protein synthesis) in the CNS under the toxic influence of MeHg. However, such suppression effect was largely blocked or alleviated by selenium. Therefore, we have provided both morphological and biochemical evidences on the protective effect of selenium on methylmercury neurotoxicity.