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)
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)
The Human Health Assessment Group in EPA's Office of Health and Environmental Assessment has evaluated dichlorophenylarsine for carcinogenicity. According to their analysis, the weight-of-evidence for dichlorophenylarsine is group D, which is based on no data evidence in humans and no data evidence in animals. As a group D chemical, dichlorophenylarsine is considered not classifiable to human carcinogenicity. Organic arsenic compounds are considered to be chemically different from the inorganic arsenic compounds such that they are assessed for carcinogenicity separately from the inorganic arsenic compounds. There are no data (weight-of-evidence group D) implicating organic arsenic compounds so that the carcinogenicity is indeterminate of this time.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌物分类
3, 无法归类其对人类的致癌性。（L135）
3, not classifiable as to its carcinogenicity to humans. (L135)
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)
The purpose of the study was to identify binding sites of organic arsenic in the erythrocyte and to explain species differences in binding. Washed erythrocytes were exposed to graded concentrations of (14)C-phenyldichloroarsine (PDA) in phosphate-buffered saline containing 0.1% glucose and 0.1% bovine serum albumin. At low phenyldichloroarsine concentrations, all cells bind the arsenical rapidly (within 10 min) and quantitatively. Human, pig, hamster, guinea pig, and mouse erythrocytes approached saturation at 0.02-0.3 mumol phenyldichloroarsine/10(9) cells, depending on the species. Saturation points correlated well with each respective species erythrocyte glutathione content. In contrast, rat erythrocytes showed no sign of saturation at phenyldichloroarsine loads as high as 3.0 mumol/10(9) cells. Hemolysates of phenyldichloroarsine-treated erythrocytes were subjected to Sephadex G-75 gel filtration chromatography. (14)C from rat hemolysate was distributed between the hemoglobin and small molecular weight (glutathione-containing) fractions. In all other species, the (14)C eluted almost exclusively with the glutathione-containing fractions. In equilibrium dialysis experiments, human hemoglobin did not bind phenyldichloroarsine, whereas rat hemoglobin bound 2 phenyldichloroarsine/mol with Kd approximately 5 m. In conclusion, glutathione is the principle binding site of phenyldichloroarsine in erythrocytes. In most species,the arsenical does not bind to hemoglobin, even though it has free (titratable) sulfhydryls considerably in excess of the glutathione concentration. In rat erythrocytes, phenyldichloroarsine binds both to glutathione and to hemoglobin.
(2-Pyridyloxy)arsines as ligands in transition metal chemistry: a stepwise As(<scp>iii</scp>) → As(<scp>ii</scp>) → As(<scp>i</scp>) reduction
作者：Robert Gericke、Jörg Wagler
DOI：10.1039/d0dt01538e
日期：——
Ph3−xAs(PyO)x (x = 2 (1), 3 (2)) have been synthesized and characterized. Reaction of 1 with [RuCl2(PPh3)3] affords complex [PhAs(μ-PyO)2RuCl2(PPh3)] (3), whereas 2 and [RuCl2(PPh3)3] react with formation of [As(μ-PyO)2RuCl(PPh3)2] (5) and [Ph3P(PyO)]Cl (6). Treatment of complex 5 with [AuCl(tht)] (tht = tetrahydrothiophene) results in liberation of tht and formation of [AuCl(As(PyO)2)RuCl(PPh3)2] (7), featuring
The pyramidal stability of dithiarsolanes and dioxarsolanes
作者：Jeremiah P. Casey、Kurt Mislow
DOI：10.1039/c2970000999b
日期：——
The barrier to inversion at arsenic in the title compounds has been shown to exceed 25 kcal mol–1, and a previous report that inversion is rapid in these compounds has thus been invalidated.
benzothieno[3,2-b]benzoheteroles containingGroup 15 (N, P, As, and Sb) and Group 16 (O, S, Se, and Te) elements were synthesized by a versatile method. X-ray analyses revealed that all the tetracyclic heteroacene skeletons were planar. A linear relationship was found between the excitation energies of Group 16-heteroacenes and their atomic radius, in contrast to Group 15-heteroacenes. Density functional
通过通用方法合成了一系列含有第15组（N，P，As和Sb）和第16组（O，S，Se和Te）元素的苯并噻吩并[3,2- b ]苯并杂环。X射线分析表明，所有的四环杂并苯骨架都是平面的。与第15族-杂蒽相比，在第16族-杂蒽的激发能和它们的原子半径之间发现线性关系。进行密度泛函理论计算和电化学测量以了解结构与光学性质之间的关系。
Heteropolytopic Arsanylarylthiolato Ligands: Cis–Trans Isomerism of Nickel(II), Palladium(II), and Platinum(II) Complexes of 1-AsPh<sub>2</sub>-2-SHC<sub>6</sub>H<sub>4</sub>
作者：Alexandra Hildebrand、Imola Sárosi、Peter Lönnecke、Luminiţa Silaghi-Dumitrescu、Menyhárt B. Sárosi、Ioan Silaghi-Dumitrescu、Evamarie Hey-Hawkins
DOI：10.1021/ic300002p
日期：2012.7.2
afforded the square-planar complexes trans-[Ni(AsS)-κ2S,As}2] (1), cis-[Pd(AsS)-κ2S,As}2] (2), trans-[Pd(AsS)-κ2S,As}2] (3), and cis-[Pt(AsS)-κ2S,As}2] (4). In the cases of nickel and platinum, only one isomer was isolated. With palladium, initially the cisisomer 2 is formed and undergoes slow isomerization to the transisomer 3 in solution. Small amounts of the trinuclear complex [PtI(1-AsPh2-μ-2-S-C6H4-κ2S
杂多芳基硫杂芳基配体1-AsPh 2 -2-SHC 6 H 4（AsSH），PhAs（2-SHC 6 H 4）2（AsS 2 H 2）和As（2-SHC 6 H 4）3（AsS 3 H 3）已经通过锂化-亲电取代程序制备。在2：1反应ASSH用的NiCl 2 ·6H 2 O，的Na 2 [的PdCl 4 ]和[PTI 2（COD）]（COD = 1,5-环辛二烯）在净的存在3得到正方形平面络合物反式- [镍（ASS）-κ 2小号，如} 2 ]（1），顺式- [钯（ASS）-κ 2小号，如} 2 ]（2），反式- [钯（ASS）-κ 2小号，如} 2 ]（3），以及顺式- [铂（ASS）-κ 2小号，正如} 2 ]（4）。在镍和铂的情况下，仅分离出一种异构体。与钯一起，最初形成顺式异构体2，并在溶液中缓慢地异构化为反式异构体3。少量三核的络合物[PTI（1- ASPH 2 -μ-2-SC
Effect of Arsenic Coordination State on the Structure, Aromaticity, and Optical Properties of Dithieno[3,2‐
<i>b</i>
:2′,3′‐
<i>d</i>
]arsoles
作者：Joshua P. Green、Arvind K. Gupta、Andreas Orthaber
DOI：10.1002/ejic.201801169
日期：2019.3.31
A silylated derivative of 4-phenyl-dithieno[3,2-b:2 ',3 '-d]arsole (DTAs) was synthesized, and the effect of coordinating of DTAs compounds to Pd on their structural and optical properties was inve ...
