锰的生物作用与神经毒性

Biological function and neurotoxicity of manganese

锰（Mn）是人体必需的微量元素，具有多种重要的生物学功能。作为丙酮酸羧化酶、精氨酸酶、葡萄糖转苷酶、过氧化物歧化酶（如MnSOD）等的辅因子或激活剂，参与碳水化舍物和蛋白代谢、氧化还原反应，调节ATP和血小板的生成。锰在自然界中丰度较高，工业应用广泛。人类在合理膳食条件下无锰缺乏的报道，然而过度暴露所致的锰中毒却较为普遍。锰中毒主要以长期、低剂量接触而引起的慢性中毒为主，导致进行性、持久性的精神、认知、运动功能损害，其早期的临床表现是神经行为功能的改变，主要表现在情感、注意力、记忆力、协调性等方面，晚期则引起类似帕金森病的锥体外系功能障碍。本篇综述将关注锰的神经毒性，及其相关生物机制。

Manganese （Mn） is an essential trace element that has a broad role in immune response, blood sugar homeostasis, adenosine triphosphate （ATP） regulation, reproduction, digestion, and bone growth. Mn has a heterogeneous distribution throughout the brain. In the normal human brain, Mn is most concentrated in the globus pallidus, caudate, and putamen and is less concentrated in cortical areas. Mn defciency, although rare, can cause developmental defects including malformation of bones, altered macromolecular metabolism, and reduced fertility. Exposure to excess levels of Mn produces cognitive, psychiatric, and motor abnormalities. We reviewed recent in vivo and ex vivo studies that have signifcantly advanced the understanding of Mn--induced neurotoxicity. These findings provide new information on mechanisms by which Mn affects behavior, neurotransmitter function, and neuropathology.