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首页> 外文学位 >Manganese toxicity: An in vivo and in vitro investigation of the relative cellular and neurotoxic effects of manganese(II) and manganese(III) exposure.
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Manganese toxicity: An in vivo and in vitro investigation of the relative cellular and neurotoxic effects of manganese(II) and manganese(III) exposure.

机译：锰毒性：体内和体外研究锰（II）和锰（III）暴露的相对细胞和神经毒性作用。

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摘要

Manganese, an essential trace element that exhibits complex redox and ligand chemistry, is also a potent neurotoxicant at elevated exposures. Elevated occupational exposures cause the neurodegenerative disease manganism, which in many ways exhibits symptoms similar to Parkinsonism. The vast majority of studies evaluating the mechanism(s) of manganese toxicity have evaluated the toxicity of divalent manganese. However, exposure to manganese through the combustion products of MMT or aerosols in occupational settings lead to exposure to manganese in a mixture of oxidation states. Most studies attempting to evaluate the toxicity of trivalent manganese have failed to assess the stability of Mn(III) in their exposure source, resulting in misleading if not invalid conclusions. Here, studies were conducted to evaluate several inorganic sources of Mn(III) and report their relative stability in aqueous solution. The relative toxicity resulting from exposures to Mn(II) and Mn(III) were subsequently investigated in three models of biological systems. We report that, in general, Mn(III) exposures are more toxic than Mn(II) exposures in simple aqueous systems, in a dopaminergic cell culture model system (PC 12's) and in a animal model (rattus species) of human manganese toxicity. Collectively, these data reflect the dynamic effects of manganese speciation in simple biological systems, and the importance of manganese oxidation/speciation state of exposure in mediating potential cellular toxicity in intact biological systems. The generally greater toxicity of Mn(III) exposures appears to be due in part to the greater relative cellular uptake of manganese when administered as Mn(III), and to a seemingly greater ability to disrupt basic cell function, such as neurotransmitter concentrations and the expression of proteins responsible for regulating iron homeostasis. This study supports concern over elevated environmental and occupational exposures to manganese that may occur in different oxidation states from combustion products of the gasoline anti-knock additive methylcyclopentadienyl manganese tricarbonyl (MMT).
机译：锰是一种表现出复杂的氧化还原和配体化学反应的必需微量元素，在暴露量增加时也是一种有效的神经毒剂。高职业暴露会引起神经退行性疾病锰症，这种疾病在许多方面表现出类似于帕金森氏症的症状。评估锰毒性机理的绝大多数研究都评估了二价锰的毒性。但是，在职业环境中通过MMT或气溶胶的燃烧产物暴露于锰会导致以氧化态的混合物暴露于锰。大多数试图评估三价锰毒性的研究都未能评估其暴露源中Mn（III）的稳定性，从而导致误导性的结论，即使不是无效的结论。在这里，进行了研究，以评估Mn（III）的几种无机来源，并报告了它们在水溶液中的相对稳定性。随后在三种生物系统模型中研究了由于暴露于Mn（II）和Mn（III）而产生的相对毒性。我们报告说，在简单的水系统中，在多巴胺能细胞培养模型系统（PC 12's）和对人类锰毒性的动物模型（rattus种）中，一般而言，Mn（III）暴露比Mn（II）暴露更具毒性。 。总的来说，这些数据反映了简单生物系统中锰物种形成的动态影响，以及锰的氧化/形态暴露状态在完整生物系统中介导潜在细胞毒性中的重要性。 Mn（III）暴露通常具有更大的毒性，这部分是由于以Mn（III）的形式施用时，锰相对细胞的摄入量更大，并且似乎具有更大的破坏基本细胞功能（如神经递质浓度和抗氧化剂）的能力。负责调节铁稳态的蛋白质的表达。这项研究支持对汽油中抗爆添加剂甲基环戊二烯基三羰基锰（MMT）的燃烧产物在不同氧化态下可能发生的锰暴露于环境和职业的关注。

著录项

  • 作者

    Reaney, Stephen Howard.;

  • 作者单位

    University of California, Santa Cruz.;

  • 授予单位 University of California, Santa Cruz.;
  • 学科 Chemistry Biochemistry.; Health Sciences Toxicology.
  • 学位 Ph.D.
  • 年度 2003
  • 页码 141 p.
  • 总页数 141
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物化学;毒物学（毒理学）;
  • 关键词

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