硝酸汞 | 10045-94-0

• 分子结构分类: 无机化合物 - 混合金属/非金属化合物 - 过渡金属氧阴离子化合物
• 中文名称: 硝酸汞
• 中文别名: 硝酸汞(2+)；硝酸汞(剧毒)；硝酸高汞
• 英文名称: Nitric acid, mercury(1+) salt (1:1)
• 英文别名: mercury;nitric acid
• CAS: 10045-94-0
• 化学式: HHgNO3
• 分子量: 263.61
• InChiKey: VRJVVIKEWDDYOG-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  -0.35
• 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
• 氢给体数：
  1
• 氢受体数：
  3

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汞离子，这一过程通过过氧化氢酶-过氧化氢途径进行。汞原子能够扩散到过氧化氢酶酶隙中，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，氧化最可能发生在所有组织中。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。摄入一定量的硝酸盐和亚硝酸盐是人类氮循环的正常部分。在适当的条件下，硝酸盐可以在胃肠道内转化为亚硝酸盐，显著增强硝酸盐的毒性。硝酸盐的主要代谢途径是转化为亚硝酸盐，然后转化为氨。亚硝酸盐、硝酸盐及其代谢物通过尿液排出体外。

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. Intake of some amount of nitrates and nitrites is a normal part of the nitrogen cycle in humans. In vivo conversion of nitrates to nitrites can occur in the gastrointestional tract under the right conditions, significantly enhancing nitrates' toxic potency. The major metabolic pathway for nitrate is conversion to nitrite, and then to ammonia. Nitrites, nitrates, and their metabolites are excreted in the urine. (L1137, A6, L7)

来源:Toxin and Toxin Target Database (T3DB)

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汞离子，这一过程通过过氧化氢酶-过氧化氢途径进行。汞原子能够扩散到过氧化氢酶酶隙中，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，氧化最可能发生在所有组织中。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。摄入一定量的硝酸盐和亚硝酸盐是人类氮循环的正常部分。在适当的条件下，硝酸盐可以在胃肠道内转化为亚硝酸盐，显著增强硝酸盐的毒性。硝酸盐的主要代谢途径是转化为亚硝酸盐，然后转化为氨。亚硝酸盐、硝酸盐及其代谢物通过尿液排出体外。

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. Intake of some amount of nitrates and nitrites is a normal part of the nitrogen cycle in humans. In vivo conversion of nitrates to nitrites can occur in the gastrointestional tract under the right conditions, significantly enhancing nitrates' toxic potency. The major metabolic pathway for nitrate is conversion to nitrite, and then to ammonia. Nitrites, nitrates, and their metabolites are excreted in the urine. (L1137, 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，汞能抑制水通道蛋白，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，并改变血脑屏障。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。硝酸盐的毒性是由于它进入体内后转化为亚硝酸盐。亚硝酸盐导致氧合血红蛋白的自动催化氧化为过氧化氢和高铁血红蛋白。这种高铁血红蛋白水平的升高被称为高铁血红蛋白血症，其特点是组织缺氧，因为高铁血红蛋白不能结合氧气。

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. Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (A2450, L1613, L7, A8, A25, A26)

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，汞能抑制水通道蛋白，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，并改变血脑屏障。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。硝酸盐的毒性是由于它进入体内后转化为亚硝酸盐。亚硝酸盐导致氧合血红蛋白的自动催化氧化为过氧化氢和高铁血红蛋白。这种高铁血红蛋白水平的升高被称为高铁血红蛋白血症，其特点是组织缺氧，因为高铁血红蛋白不能结合氧气。

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. Nitrate's toxicity is a result of it's conversion to nitrite once in the body. Nitrite causes the autocatalytic oxidation of oxyhemoglobin to hydrogen peroxide and methemoglobin. This elevation of methemoglobin levels is a condition known as methemoglobinemia, and is characterized by tissue hypoxia, as methemoglobin cannot bind oxygen. (A2450, L1613, L7, A8, A25, A26)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 致癌物分类

摄入的硝酸盐或亚硝酸盐在导致内源性亚硝化的条件下，可能对人类具有致癌性（2A组）。无机汞化合物对人类是否具有致癌性无法归类（3组）。

Ingested nitrate or nitrite under conditions that result in endogenous nitrosation is probably carcinogenic to humans (Group 2A). Inorganic mercury compounds are not classifiable as to their carcinogenicity to humans (Group 3). (L135)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 致癌物分类

摄入硝酸盐或亚硝酸盐，在导致内源性亚硝化的条件下，可能对人类具有致癌性（2A组）。无机汞化合物对人类的致癌性无法分类（3组）。

Ingested nitrate or nitrite under conditions that result in endogenous nitrosation is probably carcinogenic to humans (Group 2A). Inorganic mercury compounds are not classifiable as to their carcinogenicity to humans (Group 3). (L135)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 健康影响

汞主要影响神经系统。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。儿童中的汞中毒，即手足口病，其特征是手和脚疼痛和粉红色变色。汞中毒还可能导致亨特-拉塞尔综合症和熊本病。硝酸盐和亚硝酸盐中毒引起高铁血红蛋白血症。亚硝酸盐可能导致怀孕并发症和发育影响。它们也可能具有致癌性。

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. Nitrate and nitrite poisoning causes methemoglobinemia. Nitrites may cause pregnancy complications and developmental effects. They may also be carcinogenic. (L1137, L7)

来源:Toxin and Toxin Target Database (T3DB)