Au Catherine, Benedetto Alexandre, Aschner Michael
Center for Molecular Neuroscience, Vanderbilt University Medical Center, Nashville, TN 37232-0414, United States.
Neurotoxicology. 2008 Jul;29(4):569-76. doi: 10.1016/j.neuro.2008.04.022. Epub 2008 May 14.
Manganese (Mn) is a transition metal that is essential for normal cell growth and development, but is toxic at high concentrations. While Mn deficiency is uncommon in humans, Mn toxicity is known to be readily prevalent due to occupational overexposure in miners, smelters and possibly welders. Excessive exposure to Mn can cause Parkinson's disease-like syndrome; patients typically exhibit extrapyramidal symptoms that include tremor, rigidity and hypokinesia [Calne DB, Chu NS, Huang CC, Lu CS, Olanow W. Manganism and idiopathic parkinsonism: similarities and differences. Neurology 1994;44(9):1583-6; Dobson AW, Erikson KM, Aschner M. Manganese neurotoxicity. Ann NY Acad Sci 2004;1012:115-28]. Mn-induced motor neuron diseases have been the subjects of numerous studies; however, this review is not intended to discuss its neurotoxic potential or its role in the etiology of motor neuron disorders. Rather, it will focus on Mn uptake and transport via the orthologues of the divalent metal transporter (DMT1) and its possible implications to Mn toxicity in various categories of eukaryotic systems, such as in vitro cell lines, in vivo rodents, the fruitfly, Drosophila melanogaster, the honeybee, Apis mellifera L., the nematode, Caenorhabditis elegans and the baker's yeast, Saccharomyces cerevisiae.
锰(Mn)是一种过渡金属,对正常细胞生长和发育至关重要,但在高浓度时具有毒性。虽然锰缺乏在人类中并不常见,但由于矿工、冶炼工人以及可能还有焊工的职业性过度暴露,锰中毒已被认为很普遍。过度接触锰会导致帕金森病样综合征;患者通常表现出锥体外系症状,包括震颤、僵硬和运动迟缓[卡尔内DB,朱NS,黄CC,卢CS,奥洛诺W。锰中毒与特发性帕金森病:异同。神经病学1994;44(9):1583 - 6;多布森AW,埃里克森KM,阿斯chner M。锰神经毒性。纽约科学院学报2004;1012:115 - 28]。锰诱导的运动神经元疾病一直是众多研究的主题;然而,本综述无意讨论其神经毒性潜力或其在运动神经元疾病病因中的作用。相反,它将专注于通过二价金属转运蛋白(DMT1)的同源物进行的锰摄取和转运,以及其对各种真核系统中锰毒性的可能影响,如体外细胞系、体内啮齿动物、果蝇、黑腹果蝇、蜜蜂、意大利蜜蜂、线虫、秀丽隐杆线虫和面包酵母、酿酒酵母。
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