Ferric cacodylate | 5968-84-3

• 物质功能分类: 有机原料 - 羧酸类化合物及衍生物
• 分子结构分类: 有机化合物 - 有机金属化合物 - 有机类金属化合物
• 英文名称: Ferric cacodylate
• 英文别名: dimethylarsinate;iron(3+)
• CAS: 5968-84-3
• 化学式: C6H18As3FeO6
• 分子量: 466.81
• InChiKey: LZHICUSBBXKVSP-UHFFFAOYSA-K

物化性质

• 颜色/状态：
  YELLOWISH, AMORPHOUS POWDER
• 气味：
  ODORLESS
• 溶解度：
  6.67 G/100 CC COLD WATER; SLIGHTLY SOL IN ALCOHOL

计算性质

• 辛醇/水分配系数(LogP)：
  -1.57
• 重原子数：
  16
• 可旋转键数：
  0
• 环数：
  0.0
• sp3杂化的碳原子比例：
  1.0
• 拓扑面积：
  120
• 氢给体数：
  0
• 氢受体数：
  6

ADMET

代谢

砷主要通过吸入或摄入进入人体，其次是皮肤接触。进入人体后，砷会在全身分布，根据需要被还原成亚砷酸盐，然后通过亚砷酸盐甲基转移酶被甲基化成单甲基砷（MMA）和二甲基硅酸（DMA）。砷及其代谢物主要通过尿液排出体外。已知砷能诱导金属结合蛋白金属硫蛋白，金属硫蛋白通过结合砷和其他金属，使它们生物学上失活，并作为抗氧化剂，从而减少砷和其他金属的有毒效果。

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)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 毒性总结

砒霜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，砒霜抑制了丙酮酸脱氢酶，并通过与磷酸竞争解耦了氧化磷酸化，从而抑制了与能量相关的NAD+还原、线粒体呼吸和ATP合成。过氧化氢的产生也增加了，这可能会形成活性氧物种和氧化应激。砒霜的致癌性受到砒霜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。其他砒霜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。

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)

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

砒霜中毒可能导致多系统器官衰竭死亡，可能是由于细胞坏死而非凋亡。砒霜也是一种已知的致癌物，尤其是在皮肤癌、肝癌、膀胱癌和肺癌中。

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)

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

暴露于较低水平的砷可以导致恶心和呕吐，减少红白细胞的生产，心律异常，血管损伤，以及一种感觉。

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)

吸收、分配和排泄

观察给予口服的59Fe标记的阳离子醋酸铁(59Fe-Cac)胶体、阴离子柠檬酸铁(59Fe-Cit)胶体、阳离子59Fe-Cac复合物和阴离子59Fe-Cit复合物的大鼠，发现铁的吸收在59Fe-Cac胶体中最有效，59Fe-Cac复合物中中等，59Fe-Cit胶体中较低，而在59Fe-Cit复合物中最低。在给予59Fe-Cac胶体和59Fe-Cac复合物的大鼠中，肝脏以及循环血液中的红细胞或血红蛋白中的活性非常高，而血浆、骨髓和脾脏中的活性较低。对大鼠空肠粘膜独立暴露10分钟于Fe-Cac胶体、阴离子Fe-Cit胶体以及Fe-Cac和Fe-Cit复合物的组织化学观察显示，阳离子Fe-Cac胶体和Fe-Cac复合物附着在覆盖绒毛顶端的粘膜的腔面，其中一些铁离子进入毛细血管，而阴离子Fe-Cit胶体和复合物并未附着在上皮细胞上，而是自由存在于空肠腔内。电子显微镜揭示，Fe-Cac胶体粒子通过微绒毛网的胞吞作用被上皮细胞摄取，移动到高尔基体区域，通过胞吐作用到达细胞间隙，然后转移到基底膜并向毛细血管方向转运。

... Observation of rats given oral administration of 59Fe-labeled cationic cacodylate ferric (59Fe-Cac) colloid, anionic citrate ferric (59Fe-Cit) colloid, cationic 59Fe-Cac complex and anionic 59Fe-Cit complex revealed that iron absorption was more efficient in the 59Fe-Cac colloid, moderate in the 59Fe-Cac complex, low in the 59Fe-Cit colloid, and lowest in the 59Fe- cases given 59Fe-Cac colloid and 59Fe-Cac complex, a very high ratio activity was found in the liver and in the erythrocyte or hemoglobin in circulating blood, while the blood plasma, bone marrow, and spleen were low in activity. Histochemical observations of rat jejunal mucosa exposed independently for 10 min to the Fe-Cac colloid, anionic Fe-Cit colloid, and Fe-Cac and Fe-Cit complexes revealed that the cationic Fe-Cac colloid and Fe-Cac complex adhered to the luminal surface of the mucosa covering the apical area of villi with some ferric iron in the capillaries, while the anionic Fe-Cit colloid and complex did not adhere to the epithelial cells and were found free in the jejunal lumen. Electron microscopy revealed that Fe-Cac colloid particles were taken into epithelial cells by pinocytosis at the webs of microvilli, moved to the Golgi area, exocytosed to the intercellular spaces, and then translocated into the basement membrane toward blood capillaries.

来源:Hazardous Substances Data Bank (HSDB)