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环境毒物锰的暴露、流行病学及作用机制

Exposure, epidemiology, and mechanism of the environmental toxicant manganese.

作者信息

Chen Pan, Culbreth Megan, Aschner Michael

机构信息

Department of Molecular Pharmacology, Albert Einstein College of Medicine, Forchheimer Building, 1300 Morris Park Avenue, Bronx, NY, 10461, USA.

出版信息

Environ Sci Pollut Res Int. 2016 Jul;23(14):13802-10. doi: 10.1007/s11356-016-6687-0. Epub 2016 Apr 22.

Abstract

It has become increasingly apparent that global manganese (Mn) pollution to air and water is a significant threat to human health. Despite this recognition, research is only beginning to comprehend the detrimental effects of exposure. Mn, while essential, is particularly harmful to the central nervous system, and overexposure is symptomatic of several neurological disorders. At-risk populations have been identified, but it is still unclear whether typical exposure levels have any long-term consequences. Those at an elevated risk have diminished intellectual function, learning and memory, and mental development. While the overall mechanism of toxicity is undetermined, Mn has been found to induce oxidative stress, exacerbate mitochondrial dysfunction, dysregulate autophagy, and promote apoptosis, ultimately enhancing neurodegeneration. Extrapolation of this in vitro and in vivo data to humans is difficult. There is a definite need to correlate epidemiological studies with causative effects. It is imperative that research efforts endure, so threats are appropriately identified and exposure properly regulated.

摘要

全球空气和水受到的锰污染对人类健康构成重大威胁,这一点已日益明显。尽管人们已经认识到这一点,但相关研究才刚刚开始理解接触锰的有害影响。锰虽然必不可少,但对中枢神经系统特别有害,过度接触会引发多种神经疾病。已确定了高危人群,但典型接触水平是否会产生任何长期后果仍不清楚。高危人群的智力功能、学习和记忆以及心理发展都有所减退。虽然毒性的总体机制尚未确定,但已发现锰会诱导氧化应激、加剧线粒体功能障碍、失调自噬并促进细胞凋亡,最终加剧神经退行性变。将这些体外和体内数据外推至人类很困难。绝对有必要将流行病学研究与因果效应联系起来。必须持续进行研究工作,以便正确识别威胁并适当管控接触。

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