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真核生物中的锰转运:二价金属离子转运体1的作用

Manganese transport in eukaryotes: the role of DMT1.

作者信息

Au Catherine, Benedetto Alexandre, Aschner Michael

机构信息

Center for Molecular Neuroscience, Vanderbilt University Medical Center, Nashville, TN 37232-0414, United States.

出版信息

Neurotoxicology. 2008 Jul;29(4):569-76. doi: 10.1016/j.neuro.2008.04.022. Epub 2008 May 14.


DOI:10.1016/j.neuro.2008.04.022
PMID:18565586
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2501114/
Abstract

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.

摘要

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。

相似文献

[1]
Manganese transport in eukaryotes: the role of DMT1.

Neurotoxicology. 2008-7

[2]
SMF-1, SMF-2 and SMF-3 DMT1 orthologues regulate and are regulated differentially by manganese levels in C. elegans.

PLoS One. 2009-11-18

[3]
Iron interactions and other biological reactions mediating the physiological and toxic actions of manganese.

Biochem Pharmacol. 2003-7-1

[4]
Manganese efflux in Parkinsonism: insights from newly characterized SLC30A10 mutations.

Biochem Biophys Res Commun. 2013-1-26

[5]
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Int Rev Neurobiol. 2013

[6]
The divalent metal transporter homologues SMF-1/2 mediate dopamine neuron sensitivity in caenorhabditis elegans models of manganism and parkinson disease.

J Biol Chem. 2009-12-18

[7]
Iron mitigates DMT1-mediated manganese cytotoxicity via the ASK1-JNK signaling axis: Implications of iron supplementation for manganese toxicity.

Sci Rep. 2016-2-16

[8]
Altered manganese homeostasis: implications for BLI-3-dependent dopaminergic neurodegeneration and SKN-1 protection in C. elegans.

J Trace Elem Med Biol. 2012-5-15

[9]
SLC30A10 is a cell surface-localized manganese efflux transporter, and parkinsonism-causing mutations block its intracellular trafficking and efflux activity.

J Neurosci. 2014-10-15

[10]
Relative contribution of CTR1 and DMT1 in copper transport by the blood-CSF barrier: implication in manganese-induced neurotoxicity.

Toxicol Appl Pharmacol. 2012-3-18

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[3]
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[4]
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[5]
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Int J Mol Sci. 2023-6-24

[6]
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[7]
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[8]
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[9]
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[10]
as a Model to Study Manganese-Induced Neurotoxicity.

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本文引用的文献

[1]
Site-directed mutagenesis investigation of coupling properties of metal ion transport by DCT1.

Biochim Biophys Acta. 2008-1

[2]
High-throughput in vivo analysis of gene expression in Caenorhabditis elegans.

PLoS Biol. 2007-9

[3]
Recent progress in structure-function analyses of Nramp proton-dependent metal-ion transporters.

Biochem Cell Biol. 2006-12

[4]
Olfactory uptake of manganese requires DMT1 and is enhanced by anemia.

FASEB J. 2007-1

[5]
Upregulation of DMT1 expression in choroidal epithelia of the blood-CSF barrier following manganese exposure in vitro.

Brain Res. 2006-6-30

[6]
A manganese-enhanced diet alters brain metals and transporters in the developing rat.

Toxicol Sci. 2006-8

[7]
ZIP8, member of the solute-carrier-39 (SLC39) metal-transporter family: characterization of transporter properties.

Mol Pharmacol. 2006-7

[8]
A novel R416C mutation in human DMT1 (SLC11A2) displays pleiotropic effects on function and causes microcytic anemia and hepatic iron overload.

Blood Cells Mol Dis. 2006

[9]
Two new human DMT1 gene mutations in a patient with microcytic anemia, low ferritinemia, and liver iron overload.

Blood. 2006-5-15

[10]
Microcytic anemia and hepatic iron overload in a child with compound heterozygous mutations in DMT1 (SCL11A2).

Blood. 2006-1-1

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