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Cupric arsenite | 10290-12-7

中文名称
——
中文别名
——
英文名称
Cupric arsenite
英文别名
copper;hydrogen arsorite
Cupric arsenite化学式
CAS
10290-12-7
化学式
AsHO3*Cu
mdl
——
分子量
187.474
InChiKey
BPQWCZKMOKHAJF-UHFFFAOYSA-N
BEILSTEIN
——
EINECS
——
  • 物化性质
  • 计算性质
  • ADMET
  • 安全信息
  • SDS
  • 制备方法与用途
  • 上下游信息
  • 反应信息
  • 文献信息
  • 表征谱图
  • 同类化合物
  • 相关功能分类
  • 相关结构分类

物化性质

  • 熔点:
    decomposes [HAW93]
  • 溶解度:
    不溶于水、乙醇;溶于酸溶液
  • 物理描述:
    Copper arsenite is a fine, light-green powder. It is insoluble in water. It is very toxic by ingestion. It is used as an insecticide and fungicide.
  • 颜色/状态:
    Yellowish-green powder
  • 密度:
    greater than 1.1 at 68 °F (est) (USCG, 1999)
  • 分解:
    Decomposes at melting point.

计算性质

  • 辛醇/水分配系数(LogP):
    -3.32
  • 重原子数:
    5
  • 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:
    66.4
  • 氢给体数:
    1
  • 氢受体数:
    3

ADMET

代谢
铜主要通过消化道吸收,但也可以通过吸入和皮肤吸收。它通过基底外侧膜,可能是通过调节铜转运蛋白,并与血清白蛋白结合运输到肝脏和肾脏。肝脏是铜稳态的关键器官。在肝脏和其他组织中,铜以与金属硫蛋白、氨基酸以及与依赖铜的酶相关联的形式储存,然后分配通过胆汁排泄或并入细胞内和细胞外蛋白中。铜通过血浆中与血清白蛋白、铜蓝蛋白或低分子量复合物结合输送到外周组织。铜可能诱导金属硫蛋白和铜蓝蛋白的产生。膜结合的铜转运腺苷三磷酸酶(Cu-ATPase)将铜离子运输进出细胞。生理上正常的铜水平通过改变铜的吸收速率和数量、分布区域以及排泄来保持恒定。砷主要通过吸入或摄入吸收,其次是通过皮肤接触。然后它分布到全身,如有必要,将其还原为砒霜,然后通过砒霜甲基转移酶甲基化为单甲基砷(MMA)和二甲砷酸(DMA)。砷及其代谢物主要通过尿液排出。砷已知能诱导金属结合蛋白金属硫蛋白,通过结合砷和其他金属使它们生物活性失效,并作为抗氧化剂,从而减少砷和其他金属的有毒效果。
Copper is mainly absorbed through the gastrointestinal tract, but it can also be inhalated and absorbed dermally. It passes through the basolateral membrane, possibly via regulatory copper transporters, and is transported to the liver and kidney bound to serum albumin. The liver is the critical organ for copper homoeostasis. In the liver and other tissues, copper is stored bound to metallothionein, amino acids, and in association with copper-dependent enzymes, then partitioned for excretion through the bile or incorporation into intra- and extracellular proteins. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular-weight complexes. Copper may induce the production of metallothionein and ceruloplasmin. The membrane-bound copper transporting adenosine triphosphatase (Cu-ATPase) transports copper ions into and out of cells. Physiologically normal levels of copper in the body are held constant by alterations in the rate and amount of copper absorption, compartmental distribution, and excretion. 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, L277, L279)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
  • 毒性总结
过量的铜被隔离在肝细胞溶酶体内,在那里它与金属硫蛋白结合。铜肝毒性被认为是当溶酶体饱和并且铜在细胞核中积累,导致核损伤时发生的。这种损伤可能是由于氧化损伤,包括脂质过氧化。铜抑制了诸如葡萄糖-6-磷酸1-脱氢酶、谷胱甘肽还原酶和对氧磷酶等含有巯基团的酶,这些酶保护细胞免受自由氧自由基的损害。它还影响基因表达,并且是诸如细胞色素C氧化酶和赖氨氧化酶等氧化酶的辅因子。此外,由铜诱导的氧化应激被认为会激活酸性鞘磷脂酶,导致神经酰胺的产生,这是一种凋亡信号,同时也会引起溶血性贫血。铜诱导的呕吐是由于迷走神经的刺激。砷及其代谢物通过多种机制干扰ATP的产生。在柠檬酸循环的水平上,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+的还原、线粒体呼吸和ATP合成。过氧化氢的产生也增加了,这可能形成活性氧种和氧化应激。砷的致癌性受到砷与微管蛋白结合的影响,这导致非整倍体、多倍体和有丝分裂停止。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。
Excess copper is sequestered within hepatocyte lysosomes, where it is complexed with metallothionein. Copper hepatotoxicity is believed to occur when the lysosomes become saturated and copper accumulates in the nucleus, causing nuclear damage. This damage is possibly a result of oxidative damage, including lipid peroxidation. Copper inhibits the sulfhydryl group enzymes such as glucose-6-phosphate 1-dehydrogenase, glutathione reductase, and paraoxonases, which protect the cell from free oxygen radicals. It also influences gene expression and is a co-factor for oxidative enzymes such as cytochrome C oxidase and lysyl oxidase. In addition, the oxidative stress induced by copper is thought to activate acid sphingomyelinase, which lead to the production of ceramide, an apoptotic signal, as well as cause hemolytic anemia. Copper-induced emesis results from stimulation of the vagus nerve. 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, L277, T49, A174, L280)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
  • 致癌性证据
致癌性分类:1)人类证据:充分;2)动物证据:有限。对人类致癌风险的总体评估为第1组:对人类致癌。注意:此评估适用于整个化学物质组,而不一定适用于组内所有单个化学物质。/砷和砷化合物/
Classification of carcinogenicity: 1) evidence in humans: sufficient; 2) evidence in animals: limited. Overall summary evaluation of carcinogenic risk to humans is Group 1: Carcinogenic to humans. NOTE: This evaluation applies to the group of chemicals as a whole and not necessarily to all individual chemicals within the group. /Arsenic and arsenic compounds/
来源:Hazardous Substances Data Bank (HSDB)
毒理性
  • 致癌性证据
分类:A;人类致癌物。分类依据:基于足够的人类数据。在主要通过吸入暴露的多个人类群体中观察到了肺癌死亡率的增加。此外,在饮用含有高无机砷的饮用水的人群中,观察到了多个内部器官癌症(肝脏、肾脏、肺和膀胱)死亡率的增加以及皮肤癌发病率的增加。人类致癌性数据:充分。动物致癌性数据:不充分。/无机砷/ /基于先前的分类系统/
CLASSIFICATION: A; human carcinogen. BASIS FOR CLASSIFICATION: Based on sufficient evidence from human data. An increased lung cancer mortality was observed in multiple human populations exposed primarily through inhalation. Also, increased mortality from multiple internal organ cancers (liver, kidney, lung, and bladder) and an increased incidence of skin cancer were observed in populations consuming drinking water high in inorganic arsenic. HUMAN CARCINOGENICITY DATA: Sufficient. ANIMAL CARCINOGENICITY DATA: Inadequate. /Inorganic Arsenic/ /Based on former classification system/
来源:Hazardous Substances Data Bank (HSDB)
毒理性
  • 致癌性证据
A1:已确认的人类致癌物。/砷和无机砷化合物,如As/
A1: Confirmed human carcinogen. /Arsenic and inorganic compounds, as As/
来源:Hazardous Substances Data Bank (HSDB)
毒理性
  • 致癌性证据
评估:有足够的人类证据表明饮用水中的砷可导致膀胱癌、肺癌和皮肤癌...总体评估:饮用水中的砷对人类具有致癌性(第1组)。/饮用水中的砷/
Evaluation: There is sufficient evidence in humans that arsenic in drinking-water causes cancers of the urinary bladder, lung and skin ... Overall evaluation: Arsenic in drinking-water is carcinogenic to humans (Group 1). /Arsenic in drinking-water/
来源:Hazardous Substances Data Bank (HSDB)

安全信息

  • 危险等级:
    6.1(a)
  • 危险品运输编号:
    1586
  • 包装等级:
    II
  • 危险类别:
    6.1(a)

制备方法与用途

用途:用作分析试剂
类别:有毒物品
毒性分级:剧毒
可燃性危险特性:不可燃烧;遇酸会产生剧毒三氧化二砷;火场会产生有毒的砷氧化物烟雾
储运特性:应存放在通风、低温和干燥的库房中,并与酸类及食品分开存放运输
灭火剂:可用雾状水或砂土进行扑灭
职业标准:短期暴露极限(STEL)为 0.6 毫克/立方米(砷),时间加权平均值(TLV-TWA)为 0.2 毫克/立方米(砷)

反应信息

  • 作为反应物:
    描述:
    Cupric arsenite 作用下, 生成
    参考文献:
    名称:
    Luchinskij, G. P.; Churilkina, V. F., Zhurnal Obshchei Khimii, 1940, vol. 10, p. 1425 - 1431
    摘要:
    DOI:
  • 作为产物:
    描述:
    potassium hydrogen arsenite 、 copper(II) sulfate 生成 Cupric arsenite
    参考文献:
    名称:
    XXXIX:关于砷酸对碱和某些砷的容量
    摘要:
    DOI:
    10.1039/js8621500281
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文献信息

  • Gmelin Handbuch der Anorganischen Chemie, Gmelin Handbook: Cu: MVol.B2, 143, page 945 - 947
    作者:
    DOI:——
    日期:——
  • XXXIX.—On the capacity of arsenious acid for bases, and on certain arsenites
    作者:Charles L. Bloxam
    DOI:10.1039/js8621500281
    日期:——
  • Bloxam, C. L., Journal fuer Praktische Chemie (Leipzig), 1862, vol. 87, p. 114 - 119
    作者:Bloxam, C. L.
    DOI:——
    日期:——
  • Luchinskij, G. P.; Churilkina, V. F., Zhurnal Obshchei Khimii, <hi>1940</hi>, vol. 10, p. 1425 - 1431
    作者:Luchinskij, G. P.、Churilkina, V. F.
    DOI:——
    日期:——
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