National Institute for Minamata Disease, Minamata, Kumamoto 867-0008, Japan.
Environ Sci Technol. 2013 Mar 19;47(6):2862-8. doi: 10.1021/es304226h. Epub 2013 Feb 25.
Although many experimental studies have shown that selenium protects against methylmercury (MeHg) toxicity at different end points, the direct interactive effects of selenium and MeHg on neurons in the brain remain unknown. Our goal is to confirm the protective effects of selenium against neuronal degeneration induced by MeHg in the developing postnatal rat brain using a postnatal rat model that is suitable for extrapolating the effects of MeHg to the fetal brain of humans. As an exposure source of selenium, we used selenomethionine (SeMet), a food-originated selenium. Wistar rats of postnatal days 14 were orally administered with vehicle (control), MeHg (8 mg Hg/kg/day), SeMet (2 mg Se/kg/day), or MeHg plus SeMet coexposure for 10 consecutive days. Neuronal degeneration and reactive astrocytosis were observed in the cerebral cortex of the MeHg-group but the symptoms were prevented by coexposure to SeMet. These findings serve as a proof that dietary selenium can directly protect neurons against MeHg toxicity in the mammalian brain, especially in the developing cerebrum.
尽管许多实验研究表明，硒在不同的终点上可以保护机体免受甲基汞（MeHg）的毒性作用，但硒和 MeHg 对大脑神经元的直接相互作用仍不清楚。我们的目的是使用适合将 MeHg 对人类胎儿大脑影响外推的新生大鼠模型，确认硒对 MeHg 诱导的新生大鼠大脑神经元变性的保护作用。作为硒的暴露源，我们使用了硒代蛋氨酸（SeMet），一种来源于食物的硒。将新生 14 天的 Wistar 大鼠连续 10 天经口给予载体（对照）、MeHg（8 mg Hg/kg/天）、SeMet（2 mg Se/kg/天）或 MeHg 和 SeMet 共暴露。MeHg 组大脑皮质出现神经元变性和反应性星形胶质细胞增生，但共暴露于 SeMet 可预防这些症状。这些发现证明膳食硒可以直接保护哺乳动物大脑中的神经元免受 MeHg 的毒性作用，特别是在大脑发育过程中。
