Mercury(2+);selenium(2-) | 11138-42-4

• 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
• 英文名称: Mercury(2+);selenium(2-)
• CAS: 11138-42-4
• 化学式: HgSe
• 分子量: 279.56
• InChiKey: PZWRDGVMERHXIK-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  -0.38
• 重原子数：
  2
• 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：
  1

ADMET

代谢

汞主要通过摄入和吸入被吸收，然后通过血液流布全身，其中一部分会与血红蛋白上的巯基团结合。汞可以经过氧化变成二价汞，这一过程通过过氧化氢酶-过氧化氢途径发生。汞原子能够扩散到过氧化氢酶酶裂中，到达含有血红素环的活性位点。由于过氧化氢酶-过氧化氢途径普遍存在，氧化很可能在所有组织中发生。氧化后，汞倾向于在肾脏中积累。汞主要通过呼出和粪便排出体外。硒可能通过吸入和摄入被吸收，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。有机硒首先代谢成无机硒。无机硒逐步还原成中间体氢硒化物，然后转化为硒磷酸和硒半胱氨酸tRNA并整合入硒蛋白，或者转化为硒化物的甲基化代谢物后排入尿液中。元素硒在排泄前也会被甲基化。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。

Mercury is absorbed mainly via ingestion and inhalation, then distributed throughout the body via the bloodstream, where a portion binds to sulfhydryl groups on haemoglobin. Mercury can undergo oxidation to mercuric mercury, which takes place via the catalase-hydrogen peroxide pathway. The mercury atom is able to diffuse down the cleft in the catalase enzyme to reach the active site where the heme ring is located. Oxidation most likely occurs in all tissue, as the catalase hydrogen peroxide pathway is ubiquitous. Following oxidation, mercury tends to accumulate in the kidneys. Mercury is excreted mainly by exhalation and 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, A6, L7)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 毒性总结

汞离子与蛋白质的巯基或硫醇基团的高亲和力结合被认为是汞活性的主要机制。通过改变细胞内巯基状态，汞可以促进氧化应激、脂质过氧化、线粒体功能障碍和血红素代谢的变化。已知汞能与微囊和线粒体酶结合，导致细胞损伤和死亡。例如，汞可以抑制水通道蛋白，阻止细胞膜上的水流。它还抑制LCK蛋白，导致T细胞信号传导减少和免疫系统抑制。汞还被认为是通过作用于突触后神经元膜来抑制神经兴奋性。它还通过抑制蛋白激酶C和碱性磷酸酶来影响神经系统，这会损害脑微血管的形成和功能，以及改变血脑屏障。汞还能产生自身免疫反应，可能是通过修饰主要组织相容性复合体（MHC）II类分子、自身肽、T细胞受体或细胞表面粘附分子。硒容易在生物分子和许多生化反应中替代硫，尤其是在硒浓度高而硫浓度低的情况下。通过影响线粒体和微囊电子传输，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）似乎在蛋白质合成中随机替代甲硫氨酸。这种替代可能会影响蛋白质的结构和功能，例如，通过改变二硫键。无机硒形式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。

High-affinity binding of the divalent mercuric ion to thiol or sulfhydryl groups of proteins is believed to be the major mechanism for the activity of mercury. Through alterations in intracellular thiol status, mercury can promote oxidative stress, lipid peroxidation, mitochondrial dysfunction, and changes in heme metabolism. Mercury is known to bind to microsomal and mitochondrial enzymes, resulting in cell injury and death. For example, mercury is known to inhibit aquaporins, halting water flow across the cell membrane. It also inhibits the protein LCK, which causes decreased T-cell signalling and immune system depression. Mercury is also believed to inhibit neuronal excitability by acting on the postsynaptic neuronal membrane. It also affects the nervous system by inhibiting protein kinase C and alkaline phosphatase, which impairs brain microvascular formation and function, as well as alters the blood-brain barrier. Mercury also produces an autoimmune response, likely by modification of major histocompatibility complex (MHC) class II molecules, self peptides, T-cell receptors, or cell-surface adhesion molecules. 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, L7, A8, A25, A26)

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

水银主要影响神经系统。暴露在高水平的金属汞、无机汞或有机汞中可能会永久性地损害大脑、肾脏和发育中的胎儿。对大脑功能的影响可能导致易怒、害羞、震颤、视力或听力改变以及记忆问题。儿童的水银中毒，称为手足口病，其特征是手和脚疼痛和粉红色变色。水银中毒还可能引起亨特-拉塞尔综合症和熊本病。长期口腔暴露于高浓度的硒化合物会产生一种称为硒中毒的疾病。硒中毒的主要症状是脱发、指甲脆弱和神经系统异常（如四肢麻木和其他奇怪的感觉）。动物研究已经表明，硒也可能影响精子生产和女性的生殖周期。

Mercury mainly affects the nervous system. Exposure to high levels of metallic, inorganic, or organic mercury can permanently damage the brain, kidneys, and developing fetus. Effects on brain functioning may result in irritability, shyness, tremors, changes in vision or hearing, and memory problems. Acrodynia, a type of mercury poisoning in children, is characterized by pain and pink discoloration of the hands and feet. Mercury poisoning can also cause Hunter-Russell syndrome and Minamata disease. Chronic oral exposure to high concentrations of selenium compounds can produce a disease called selenosis. The major signs of selenosis are hair loss, nail brittleness, and neurological abnormalities (such as numbness and other odd sensations in the extremities). Animal studies have shown that selenium may also affect sperm production and the female reproductive cycle. (L619, L7)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 暴露途径

口服（L7）；吸入（L7）；皮肤给药（L7）

Oral (L7) ; inhalation (L7); dermal (L7)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 症状

常见症状包括周围神经病变（表现为感觉异常、瘙痒、灼热或疼痛）、皮肤变色（如红脸颊、指尖和脚趾）、水肿（肿胀）和脱屑（死皮成层脱落）。短期口服高浓度的硒可能导致恶心、呕吐和腹泻。短暂接触空气中的元素硒或二氧化硒高浓度可能引起呼吸道刺激、支气管炎、呼吸困难以及胃痛。长期接触这两种空气传播形式可能导致呼吸道刺激、支气管痉挛和咳嗽。（L619, A5）

Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers). Short-term oral exposure to high concentrations of selenium may cause nausea, vomiting, and diarrhea. Brief exposures to high levels of elemental selenium or selenium dioxide in air can result in respiratory tract irritation, bronchitis, difficulty breathing, and stomach pains. Longer-term exposure to either of these air-borne forms can cause respiratory irritation, bronchial spasms, and coughing. (L619, A5)

来源:Toxin and Toxin Target Database (T3DB)