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本文引用的文献

1
The inhibitory effect of manganese on acetylcholinesterase activity enhances oxidative stress and neuroinflammation in the rat brain.锰对乙酰胆碱酯酶活性的抑制作用增强了大鼠大脑中的氧化应激和神经炎症。
Toxicology. 2012 Feb 26;292(2-3):90-8. doi: 10.1016/j.tox.2011.11.017. Epub 2011 Dec 3.
2
Regional cerebral metabolism in mouse under chronic manganese exposure: implications for manganism.慢性锰暴露下小鼠的区域性脑代谢:对锰中毒的影响。
Neurochem Int. 2012 Jan;60(2):177-85. doi: 10.1016/j.neuint.2011.10.016. Epub 2011 Nov 13.
3
Interactions between excessive manganese exposures and dietary iron-deficiency in neurodegeneration.锰暴露过度与神经退行性变中铁缺乏症的相互作用。
Environ Toxicol Pharmacol. 2005 May;19(3):415-21. doi: 10.1016/j.etap.2004.12.053.
4
Manganese and its role in Parkinson's disease: from transport to neuropathology.锰及其在帕金森病中的作用:从转运到神经病理学。
Neuromolecular Med. 2009;11(4):252-66. doi: 10.1007/s12017-009-8083-0.
5
Manganese exposure is cytotoxic and alters dopaminergic and GABAergic neurons within the basal ganglia.锰暴露具有细胞毒性,并会改变基底神经节内的多巴胺能神经元和γ-氨基丁酸能神经元。
J Neurochem. 2009 Jul;110(1):378-89. doi: 10.1111/j.1471-4159.2009.06145.x. Epub 2009 May 5.
6
Manganese-enhanced MRI: an exceptional tool in translational neuroimaging.锰增强磁共振成像:转化神经影像学中的一种卓越工具。
Schizophr Bull. 2008 Jul;34(4):595-604. doi: 10.1093/schbul/sbn056. Epub 2008 Jun 11.
7
Manganese: recent advances in understanding its transport and neurotoxicity.锰:在理解其转运与神经毒性方面的最新进展
Toxicol Appl Pharmacol. 2007 Jun 1;221(2):131-47. doi: 10.1016/j.taap.2007.03.001. Epub 2007 Mar 12.
8
Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration.铝、锰、铁及其他疑似导致金属诱导神经退行性变的金属的血脑屏障通量。
J Alzheimers Dis. 2006 Nov;10(2-3):223-53. doi: 10.3233/jad-2006-102-309.
9
Manganese neurotoxicity: a focus on the neonate.锰神经毒性:聚焦新生儿
Pharmacol Ther. 2007 Feb;113(2):369-77. doi: 10.1016/j.pharmthera.2006.09.002. Epub 2006 Sep 22.
10
The effects of manganese on glutamate, dopamine and gamma-aminobutyric acid regulation.锰对谷氨酸、多巴胺和γ-氨基丁酸调节的影响。
Neurochem Int. 2006 May-Jun;48(6-7):426-33. doi: 10.1016/j.neuint.2005.10.012. Epub 2006 Feb 28.

锰改变了老鼠大脑中的氨基酸水平。

Manganese alters rat brain amino acids levels.

机构信息

I-Med.UL, Department of Toxicology and Food Sciences, Faculty of Pharmacy, University of Lisbon, Lisbon, Portugal.

出版信息

Biol Trace Elem Res. 2012 Dec;150(1-3):337-41. doi: 10.1007/s12011-012-9504-8. Epub 2012 Sep 13.

DOI:10.1007/s12011-012-9504-8
PMID:22971893
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3511624/
Abstract

Manganese (Mn) is an essential element and it acts as a cofactor for a number of enzymatic reactions, including those involved in amino acid, lipid, protein, and carbohydrate metabolism. Excessive exposure to Mn can lead to poisoning, characterized by psychiatric disturbances and an extrapyramidal disorder. Mn-induced neuronal degeneration is associated with alterations in amino acids metabolism. In the present study, we analyzed whole rat brain amino acid content subsequent to four or eight intraperitoneal injections, with 25 mg MnCl₂/kg/day, at 48-h intervals. We noted a significant increase in glycine brain levels after four or eight Mn injections (p < 0.05 and p < 0.01, respectively) and arginine also after four or eight injections (p < 0.001). Significant increases were also noted in brain proline (p < 0.01), cysteine (p < 0.05), phenylalanine (p < 0.01), and tyrosine (p < 0.01) levels after eight Mn injections vs. the control group. These findings suggest that Mn-induced alterations in amino acid levels secondary to Mn affect the neurochemical milieu.

摘要

锰(Mn)是一种必需元素,它作为许多酶反应的辅助因子,包括涉及氨基酸、脂质、蛋白质和碳水化合物代谢的反应。过量暴露于锰会导致中毒,其特征为精神障碍和锥体外系障碍。锰诱导的神经元变性与氨基酸代谢的改变有关。在本研究中,我们在 48 小时的间隔内,每天通过腹腔内注射 25mg MnCl₂/kg 对大鼠进行四次或八次,随后分析了整个大鼠大脑中的氨基酸含量。我们发现,在进行四次或八次锰注射后,大脑中的甘氨酸水平显著增加(p<0.05 和 p<0.01),精氨酸也在四次或八次注射后显著增加(p<0.001)。在八次锰注射后,大脑中的脯氨酸(p<0.01)、半胱氨酸(p<0.05)、苯丙氨酸(p<0.01)和酪氨酸(p<0.01)水平也显著增加,与对照组相比。这些发现表明,锰诱导的氨基酸水平改变会影响神经化学环境。