| 12299-98-8

• 分子结构分类: 无机化合物 - 混合金属/非金属化合物 - 各种混合金属/非金属
• CAS: 12299-98-8
• 化学式: MnSe2
• 分子量: 212.88
• InChiKey: KDAKOPXAEMJUSU-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  -0.76
• 重原子数：
  3
• 可旋转键数：
  0
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  0
• 氢给体数：
  0
• 氢受体数：
  0

ADMET

代谢

锰主要通过摄入被吸收，但也可以通过吸入。它在血浆中与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，尽管它倾向于在肝脏、胰腺和肾脏中积累更多。锰能够存在于多种氧化状态，并且据信在体内会发生氧化状态的变化。锰的氧化状态可以影响组织的毒代动力学行为，甚至可能影响毒性。锰主要通过粪便排出。硒可以通过吸入和摄入被吸收，而一些硒化合物也可能通过皮肤吸收。一旦进入体内，硒主要分布到肝脏和肾脏。硒是一种必需的微量元素，是谷胱甘肽过氧化物酶、碘甲状腺原氨酸5'-脱碘酶和硫氧还蛋白还原酶的组成部分。有机硒首先代谢为无机硒。无机硒逐步还原为中间氢硒化物，然后转化为硒磷酸和硒半胱氨酸tRNA并被结合到硒蛋白中，或者转化为硒化物的甲基化代谢物后排入尿液中。元素硒在排出前也会甲基化。硒主要通过尿液和粪便排出，但某些硒化合物也可能通过呼出。

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. Manganese is capable of existing in a number of oxidation states and is believed to undergo changes in oxidation state within the body. Manganese oxidation state can influence tissue toxicokinetic behavior, and possibly toxicity. Manganese is excreted primarily in the faeces. Selenium may be absorbed through inhalation and ingestion, while some selenium compounds may also be absorbed dermally. Once in the body, selenium is distributed mainly to the liver and kidney. Selenium is an essential micronutrient and is a component of glutathione peroxidase, iodothyronine 5'-deiodinases, and thioredoxin reductase. Organic selenium is first metabolized into inorganic selenium. Inorganic selenium is reduced stepwise to the intermediate hydrogen selenide, which is either incorporated into selenoproteins after being transformed to selenophosphate and selenocysteinyl tRNA or excreted into the urine after being transformed into methylated metabolites of selenide. Elemental selenium is also methylated before excretion. Selenium is primarily eliminated in the urine and feces, but certain selenium compounds may also be exhaled. (L619, L228)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 毒性总结

锰是一种细胞毒素，可以损害运输系统、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)增强了各种细胞内儿茶酚胺的自动氧化或转化，导致自由基、活性氧种和其他细胞毒素代谢物的产生增加，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。硒可以轻易地替代生物分子中的硫，在许多生化反应中尤其如此，特别是当硒的浓度高而硫的浓度低时。通过影响线粒体和微粒体电子传输，使细胞呼吸中氧化反应所需的巯基酶失活，这可能导致急性硒中毒。硒代甲硫氨酸（一种常见的有机硒化合物）似乎也随机地替代蛋白质合成中的甲硫氨酸。这种替代可能会影响蛋白质的结构和功能性，例如，通过改变二硫键。无机形式的硒似乎通过氧化还原催化与组织巯基反应，产生活性氧种并通过氧化应激造成损害。

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. Selenium readily substitutes for sulfur in biomolecules and in many biochemical reactions, especially when the concentration of selenium is high and the concentration of sulfur is low. Inactivation of the sulfhydryl enzymes necessary for oxidative reactions in cellular respiration, through effects on mitochondrial and microsomal electron transport, might contribute to acute selenium toxicity. Selenomethionine (a common organic selenium compound) also appears to randomly substitute for methionine in protein synthesis. This substitution may affect the structure and functionability of the protein, for example, by altering disulfide bridges. Inorganic forms of selenium appear to react with tissue thiols by redox catalysis, resulting in formation of reactive oxygen species and causing damage by oxidative stress. (L619, L228)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 致癌物分类

3, 其对人类致癌性无法分类。

3, not classifiable as to its carcinogenicity to humans. (L135)

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。这种症状组合在足够严重时被称为“锰中毒”。

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（L619）；吸入（L619）；皮肤给药（L619）

Oral (L619) ; inhalation (L619) ; dermal (L619)

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)