Organic mercury is absorbed mainly by the gastrointestinal tract, then distributed throughout the body via the bloodstream. Organic mercury complexes with free cysteine and the cysteine and sulfhydryl groups on proteins such as haemoglobin. These complexes are able to mimic methionine and thus be transported throughout the body, including through the blood-brain barrier and placenta. Organic mercury is metabolized into inorganic mercury, which is eventually excreted in the urine and faeces. (T11)
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. Organic mercury exerts developmental effects by binding to tubulin, preventing microtubule assembly and causing mitotic inhibition. 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. (L7, A8, A25, A26)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌物分类
无致癌性迹象（未被国际癌症研究机构列名）。
No indication of carcinogenicity (not listed by IARC). (L135)
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. (L7)
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). (A5)
At 3 month intervals up to 24 months, the mercury content of organs, urine and feces of young male rats was measured following oral administration of Ruberon (lignisan), and Sanmicron (PMA) twice weekly in a dose of 1/100 LD50. In the group given Sanmicron, 78.5 to 99.5% of the dose was excreted. Mercury accumulated in the kidneys, with a peak concentration occurring at 21 months. Those animals receiving Ruberon excreted 67.2 to 78.2% of the dose, and accumulated mercury in the kidneys, liver, blood, and hair. The accumulated amounts of mercury in the kidneys after Ruberon continued to rise up to 18 months and were about twice as high as those for the arylmercurial. /Mercuric pesticides/
At 3 month intervals up to 24 months, the mercury content of organs, urine and feces of young male rats was measured following oral administration of Ruberon (lignisan), and Sanmicron (PMA) twice weekly in a dose of 1/100 LD50. In the group given Sanmicron, 78.5 to 99.5% of the dose was excreted. Mercury accumulated in the kidneys, with a peak concentration occurring at 21 months. Those animals receiving Ruberon excreted 67.2 to 78.2% of the dose, and accumulated mercury in the kidneys, liver, blood, and hair. The accumulated amounts of mercury in the kidneys after Ruberon continued to rise up to 18 months and were about twice as high as those for the arylmercurial. /Mercuric pesticides/
