Tricarbonyl-(methylcyclopentadienyl)-manga-nese

• 分子结构分类: 有机化合物 - 碳氢化合物 - 芳香烃
• 英文名称: Tricarbonyl-(methylcyclopentadienyl)-manga-nese
• 化学式: C9H7MnO3-
• 分子量: 218.09
• InChiKey: IYSGJCJSRBFZSZ-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  1.6
• 重原子数：
  13
• 可旋转键数：
  0
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.11
• 拓扑面积：
  3
• 氢给体数：
  0
• 氢受体数：
  4

ADMET

代谢

锰主要通过摄入被吸收，但也可以通过吸入。它会在血浆中与α-2-巨球蛋白、白蛋白或转铁蛋白结合，并分布到大脑和所有其他哺乳动物组织中，尽管它倾向于在肝脏、胰腺和肾脏中积累更多。MMT通过细胞色素P-450酶代谢为羟基甲基环戊二烯基三羰基锰和羧基环戊二烯基三羰基锰。这些代谢物通过尿液和粪便排出。(L228)

Manganese is absorbed mainly via ingestion, but can also be inhaled. It binds to alpha-2-macroglobulin, albumin, or transferrin in the plasma and is distributed to the brain and all other mammalian tissues, though it tends to accumulate more in the liver, pancreas, and kidney. MMT is metabolized by cytochrome P-450 enzymes into hydroxylmethylcyclopentadienyl manganese tricarbonyl and carboxycyclopentadienyl manganese tricarbonyl. These metabolites are excreted in the urine and faeces. (L228)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 毒性总结

锰是一种细胞毒素，能够损害运输系统、酶活性和受体功能。它主要针对中枢神经系统，尤其是基底神经节中的苍白球。人们认为锰离子Mn(II)增强了各种胞内儿茶酚胺的自动氧化或转换，导致自由基、活性氧物种和其他细胞毒素代谢产物的产生增加，同时细胞抗氧化防御机制的耗尽，导致氧化损伤和选择性破坏多巴胺能神经元。除了多巴胺，还认为锰会干扰其他神经递质，如GABA和谷氨酸。为了产生氧化损伤，锰必须首先克服抗氧化酶超氧化物歧化酶。Mn(II)的神经毒性还与其在生理条件下替代Ca(II)的能力有关。它可以通过钙单向转运体进入线粒体并抑制线粒体氧化磷酸化。它还可能抑制Ca(II)的外流，这可能导致线粒体膜完整性的丧失。Mn(II)已被证明能显著抑制线粒体顺乌头酸酶活性，改变氨基酸代谢和细胞铁稳态。

Manganese is a cellular toxicant that can impair transport systems, enzyme activities, and receptor functions. It primarily targets the central nervous system, particularily the globus pallidus of the basal ganglia. It is believed that the manganese ion, Mn(II), enhances the autoxidation or turnover of various intracellular catecholamines, leading to increased production of free radicals, reactive oxygen species, and other cytotoxic metabolites, along with a depletion of cellular antioxidant defense mechanisms, leading to oxidative damage and selective destruction of dopaminergic neurons. In addition to dopamine, manganese is thought to perturbations other neurotransmitters, such as GABA and glutamate. In order to produce oxidative damage, manganese must first overwhelm the antioxidant enzyme manganese superoxide dismutase. The neurotoxicity of Mn(II) has also been linked to its ability to substitute for Ca(II) under physiological conditions. It can enter mitochondria via the calcium uniporter and inhibit mitochondrial oxidative phosphorylation. It may also inhibit the efflux of Ca(II), which can result in a loss of mitochondrial membrane integrity. Mn(II) has been shown to inhibit mitochondrial aconitase activity to a significant level, altering amino acid metabolism and cellular iron homeostasis. (L228)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 致癌物分类

对人类无致癌性（未列入国际癌症研究机构IARC清单）。

No indication of carcinogenicity to humans (not listed by IARC).

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 健康影响

锰主要影响神经系统，可能导致行为改变和其他神经系统效应，包括动作可能变得缓慢和笨拙。这些症状足够严重时，被称为“锰症”。(L228)

Manganese mainly affects the nervous system and may cause behavioral changes and other nervous system effects, which include movements that may become slow and clumsy. This combination of symptoms when sufficiently severe is referred to as “manganism”. (L228)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 暴露途径

口服（L228）；吸入（L228）

Oral (L228) ; inhalation (L228)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 症状

锰主要影响神经系统，可能导致行为改变和其他神经系统效应，包括动作可能变得缓慢和笨拙。这些症状足够严重时，被称为“锰症”。(L228)

Manganese mainly affects the nervous system and may cause behavioral changes and other nervous system effects, which include movements that may become slow and clumsy. This combination of symptoms when sufficiently severe is referred to as “manganism”. (L228)

来源:Toxin and Toxin Target Database (T3DB)