蹄镉汞 | 29870-72-2

• 分子结构分类: 无机化合物 - 混合金属/非金属化合物 - 类金属盐
• 中文名称: 蹄镉汞
• 中文别名: 碲镉汞晶体
• 英文名称: cadmium;tellanylidenemercury
• CAS: 29870-72-2
• 化学式: CdHgTe
• 分子量: 440.6
• InChiKey: MCMSPRNYOJJPIZ-UHFFFAOYSA-N

物化性质

• 熔点：
  670 °C
• 稳定性/保质期：

  Hg1－xCdxTe晶体是一种直接跃迁型半导体，它是HgTe-CdTe赝二元系化合物半导体合金材料。这种材料具有本征载流子浓度低、电子迁移率高、电子与空穴迁移率比大、光吸收系数大、热激发速率小、电子有效质量小及热膨胀系数接近硅等特点。其导电类型可通过组分偏离或掺杂来调节。禁带宽度Eg是组分x和温度T的函数，通过调整x和T，Eg可以从半金属HgTe（Eg＝－0.3eV）变化至半导体CdTe（Eg＝1.648eV），从而覆盖1～25μm的整个红外区域。此外，Hg1－xCdxTe的静电介电常数约为14～17，高频介电常数则为10～12.5，并随组分变化而有所不同。

计算性质

• 辛醇/水分配系数(LogP)：
  -0.39
• 重原子数：
  3
• 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：
  0

ADMET

代谢

镉和汞可能通过口服、吸入和皮肤途径被吸收。汞通过血液流传遍全身，其中一部分与血红蛋白上的巯基团结合。汞可以经过氧化转化为汞离子，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。汞主要通过呼气和粪便排出体外。镉最初与金属硫蛋白和清蛋白结合，并主要运输到肾脏和肝脏。当镉的浓度超过可用金属硫蛋白的浓度时，就会观察到毒性效应，而且已经证明镉-金属硫蛋白复合物可能具有损害性。镉不为人所知的是进行任何直接的代谢转化，并以原样主要在尿液中排出。

Cadmium and mercury may be absorbed from oral, inhalation, and dermal routes. Mercury is 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. Cadmium initially binds to metallothionein and albumin and is transported mainly to the kidney and liver. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Cadmium is not known to undergo any direct metabolic conversion and is excreted unchanged, mainly in the urine. (L6, 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。镉最初与金属硫蛋白结合并被运输到肾脏。当镉的浓度超过可用金属硫蛋白时，观察到毒性效应，而且已经表明镉-金属硫蛋白复合物可能具有损害性。镉在肾脏中的积累导致重要低分子和高分子蛋白的排泄增加。镉是锌的高亲和力类似物，并能干扰其生物过程。它还与雌激素受体结合并激活它，可能刺激某些类型的癌细胞生长并导致其他雌激素效应，如生殖功能障碍。镉通过激活丝裂原活化蛋白激酶引起细胞凋亡。

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. Cadmium initially binds to metallothionein and is transported to the kidney. Toxic effects are observed once the concentration of cadmium exceeds that of available metallothionein, and it has also been shown that the cadmium-metallothionein complex may be damaging. Accumulation of cadmium in the kidney results in increased excretion of vital low and high weight molecular proteins. Cadmium is a high affinity zinc analog and can interfere in its biological processes. It also binds to and activates the estrogen receptor, likely stimulating the growth of certain types of cancer cells and causing other estrogenic effects, such as reproductive dysfunction. Cadmium causes cell apoptosis by activating mitogen-activated protein kinases. (L7, A8, L8, A18, A19, A25, A26, A28)

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

水银主要影响神经系统。接触高水平的金属汞、无机汞或有机汞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。儿童的水俣病是一种由水银中毒引起的疾病，其特点是手和脚疼痛和发红。水银中毒还可能引起亨特-拉塞尔综合症和熊本病。长期暴露在镉烟雾中会引起化学性肺炎、肺水肿以及诸如支气管炎和肺气肿等肺部疾病。镉还会在肾脏中积累，造成永久性损害。还会发生骨密度流失。(L6, L7)

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 exposure to cadmium fumes can cause chemical pneumonitis, pulmonary edema, and lung diseases such as bronchitis and emphysema. Cadmium also accumulates in the kidneys, causing permanent damage. Loss of bone density also occurs. (L6, 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

汞中毒的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（如面颊、指尖和趾尖呈现粉红色）、水肿（肿胀）以及脱皮（死皮成层脱落）。急性吸入镉烟尘会导致金属烟雾热，其特点是寒战、发热、头痛、乏力、鼻喉干燥、胸痛和咳嗽。摄入镉会导致呕吐和腹泻。

Common symptoms of mercury poisoning 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). Acute inhalation of cadmium fumes results in metal fume fever, which is characterized by chills, fever, headache, weakness, dryness of the nose and throat, chest pain, and coughing. Ingestion of cadmium causes vomiting and diarrhea. (L6, A5)

来源:Toxin and Toxin Target Database (T3DB)

制备方法与用途

合成制备方法

Hg1－xCdxTe

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