二砷酸三镍 | 13477-70-8

• 分子结构分类: 无机化合物 - 混合金属/非金属化合物 - 过渡金属氧阴离子化合物
• 中文名称: 二砷酸三镍
• 中文别名: 二(偶砷酸)三镍
• 英文名称: Trinickel bis(arsenate)
• 英文别名: arsoric acid;nickel
• CAS: 13477-70-8
• 化学式: AsH3NiO4
• 分子量: 200.637
• InChiKey: ZIPTVBOPGBCBMU-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  -2.17
• 重原子数：
  6
• 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：
  77.8
• 氢给体数：
  3
• 氢受体数：
  4

ADMET

代谢

镍主要通过肺和胃肠吸收进入人体。一旦进入人体，它会进入血液，与白蛋白、L-组氨酸和α2-巨球蛋白结合。镍倾向于积累在肺、甲状腺、肾脏、心脏和肝脏中。被吸收的镍通过尿液排出，而未被吸收的镍则通过粪便排出。砷主要通过吸入或摄入吸收，其次是通过皮肤接触。然后它被分布到全身，如果需要，它会被还原成亚砷酸盐，然后通过砷酸甲基转移酶甲基化成单甲基砷（MMA）和二甲砷酸（DMA）。砷及其代谢物主要通过尿液排出。已知砷可以诱导金属结合蛋白金属硫蛋白，它通过结合砷和其他金属并使其生物活性失效，以及作为抗氧化剂的作用，从而减少砷和其他金属的有毒效果。

Nickel is absorbed mainly through the lungs and gastrointestinal tract. Once in the body it enters the bloodstream, where it binds to albumin, L-histidine, and _2-macroglobulin. Nickel tends to accumulate in the lungs, thyroid, kidney, heart, and liver. Absorbed nickel is excreted in the urine, wherease unabsorbed nickel is excreted in the faeces. Arsenic is absorbed mainly by inhalation or ingestion, as to a lesser extent, dermal exposure. It is then distributed throughout the body, where it is reduced into arsenite if necessary, then methylated into monomethylarsenic (MMA) and dimethylarsenic acid (DMA) by arsenite methyltransferase. Arsenic and its metabolites are primarily excreted in the urine. Arsenic is known to induce the metal-binding protein metallothionein, which decreases the toxic effects of arsenic and other metals by binding them and making them biologically inactive, as well as acting as an antioxidant. (L20, L41)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 毒性总结

镍已知可以在某些酶中替代其他必需元素，如钙调神经蛋白。它具有基因毒性，一些镍化合物已被证明可以促进细胞增殖。镍对染色质蛋白具有较高的亲和力，特别是组蛋白和精蛋白。镍离子与异染色质的结合会导致包括浓缩、DNA过度甲基化、基因沉默以及组蛋白乙酰化抑制等一系列改变，这些都已被证明会干扰基因表达。镍还被证明可以改变几个转录因子，包括低氧诱导转录因子、激活转录因子和NF-KB转录因子。还有证据表明，镍离子通过直接抑制DNA修复酶或与锌离子竞争结合锌指DNA结合蛋白，从而阻碍DNA修复。镍离子还可以与多种细胞配体结合，包括氨基酸、肽和蛋白质，从而产生氧气自由基，诱导碱基损伤、DNA链断裂和DNA蛋白质交联。砷及其代谢物通过多种机制干扰ATP的产生。在柠檬酸循环层面，砷抑制丙酮酸脱氢酶，并通过与磷酸竞争，解偶联氧化磷酸化，从而抑制与能量相关的NAD+还原、线粒体呼吸和ATP合成。过氧化氢的产生也增加，可能形成活性氧物种和氧化应激。砷的致癌性受到砷与微管蛋白结合的影响，导致非整倍体、多倍体和有丝分裂停滞。其他砷蛋白靶点的结合也可能导致DNA修复酶活性改变、DNA甲基化模式改变和细胞增殖。(T1, A17, L41, A40)

Nickel is known to substitute for other essential elements in certain enzmes, such as calcineurin. It is genotoxic, and some nickel compounds have been shown to promote cell proliferation. Nickel has a high affinity for chromatin proteins, particularly histones and protamines. The complexing of nickel ions with heterochromatin results in a number of alterations including condensation, DNA hypermethylation, gene silencing, and inhibition of histone acetylation, which have been shown to disturb gene expression. Nickel has also been shown to alter several transcription factors, including hypoxia-inducible transcription factor, activating transcription factor, and NF-KB transcription factor. There is also evidence that nickel ions inhibit DNA repair, either by directly inhibiting DNA repair enzymes or competing with zinc ions for binding to zinc-finger DNA binding proteins, resulting in structural changes in DNA that prevent repair enzymes from binding. Nickel ions can also complex with a number of cellular ligands including amino acids, peptides, and proteins resulting in the generation of oxygen radicals, which induce base damage, DNA strand breaks, and DNA protein crosslinks. Arsenic and its metabolites disrupt ATP production through several mechanisms. At the level of the citric acid cycle, arsenic inhibits pyruvate dehydrogenase and by competing with phosphate it uncouples oxidative phosphorylation, thus inhibiting energy-linked reduction of NAD+, mitochondrial respiration, and ATP synthesis. Hydrogen peroxide production is also increased, which might form reactive oxygen species and oxidative stress. Arsenic's carginogenicity is influenced by the arsenical binding of tubulin, which results in aneuploidy, polyploidy and mitotic arrests. The binding of other arsenic protein targets may also cause altered DNA repair enzyme activity, altered DNA methylation patterns and cell proliferation. (T1, A17, L41, A40)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 致癌物分类

1, 对人类致癌。

1, carcinogenic to humans. (L135)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 健康影响

镍对人类最常见的有害健康影响是过敏反应。这通常表现为皮疹，尽管有些人会经历哮喘发作。长期吸入镍会导致慢性支气管炎和肺功能下降，以及损害鼻咽腔。过量摄入镍会损害胃、血液、肝脏、肾脏和免疫系统，并对生殖和发育产生不利影响。砷中毒可能导致多系统器官衰竭死亡，可能是由于坏死的细胞死亡，而不是凋亡。砷也是一种已知的致癌物，尤其是在皮肤、肝脏、膀胱和肺癌中。

The most common harmful health effect of nickel in humans is an allergic reaction. This usually manifests as a skin rash, although some people experience asthma attacks. Long term inhahation of nickel causes chronic bronchitis and reduced lung function, as well as damage to the naval cavity. Ingestion of excess nickel results in damage to the stomach, blood, liver, kidneys, and immune system, as well as having adverse effects on reproduction and development. Arsenic poisoning can lead to death from multi-system organ failure, probably from necrotic cell death, not apoptosis. Arsenic is also a known carcinogen, esepcially in skin, liver, bladder and lung cancers. (T1, L20, L41)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 暴露途径

口服（L2）；吸入（L2）；皮肤（L2）

Oral (L2) ; inhalation (L2) ; dermal (L2)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 症状

镍中毒的症状包括头痛、恶心、呕吐、眩晕、易怒和睡眠困难，随后可能出现胸痛、出汗、心跳加速和干咳。暴露于较低水平的砷可能导致恶心和呕吐、红白细胞生成减少、心律异常、血管损伤和异常感觉。

Symptoms of nickel poisoning include headache, nausea, vomiting, dizziness, irritability, and difficulty sleeping, followed by chest pains, sweating, rapid heart beat, and a dry cough. Exposure to lower levels of arsenic can cause nausea and vomiting, decreased production of red and white blood cells, abnormal heart rhythm, damage to blood vessels, and a sensation of

来源:Toxin and Toxin Target Database (T3DB)

安全信息

• 危险等级：
  6.1(a)
• 包装等级：
  II
• 危险类别：
  6.1(a)