Methylmercury, also

Mercury has a great affinity for sulfydryl moieties and, hence, binds and inactivates a variety of enzymes. Methylmercury also initiates lipid peroxidation, which can produce alterations in cell membranes. Mercury damages the microtubules in the brain by reacting with the protein tubilin. 

Breathing in or swallowing large amounts of methylmercury also results in some of the mercury moving into the brain and affecting the nervous system. Inorganic mercury salts, such as mercuric chloride, do not enter the brain as readily as methylmercury or metallic mercury vapor. 

Mercury is unusual in its ability to induce delayed neurological effects. This is especially prevalent with exposure to alkyl mercury compounds. In such cases, the onset of adverse effects may be delayed for months after the initial exposure. The delayed effects of methyl- and dimethylmercury reported in human poisonings are thought, in part, to result from binding to red blood cells, and subsequent slow release. Methylmercury also forms a complex in plasma with the amino acid cysteine, which is structurally similar to the essential amino acid methionine (Aschner and Clarkson 1988). Clarkson (1995) proposed that methylmercury can cross the blood-brain barrier "disguised" as an amino acid via a carrier-mediated system (i.e., transport is not solely the result of methylmercury s lipid solubility). 

Microbial processes can also detoxify mercury ions and organic compounds by reducing the mercury to the elemental form, which is volatile (86). This certainly reduces the environmental impact of compounds such as methylmercury, however, such a bioprocess would have to include a mercury capture system before it could be exploited on a large scale with pubHc support. 

Alkyl mercury compounds in the blood stream are found mainly in the blood cehs, and only to a smah extent in the plasma. This is probably the result of the greater stabhity of the alkyl mercuric compounds, as well as their pecuflar solubiUty characteristics. Alkyl mercury compounds affect the central nervous system and accumulate in the brain (17,18). Elimination of alkyl mercury compounds from the body is somewhat slower than that of inorganic mercury compounds and the aryl and alkoxy mercurials. Methylmercury is eliminated from humans at a rate indicating a half-life of 50—60 d (19) inorganic mercurials leave the body according to a half-life pattern of 30—60 d (20). Elimination rates are dependent not only on the nature of the compound but also on the dosage, method of intake, and the rate of intake (21,22). 

Metals and metalloids that form alkyl compounds, eg, methylmercury and methylarsenic acid, tributjltin, deserve special concern because these compounds are volatile and accumulate in cells they are poisonous to the central nervous system of higher organisms. Because methylmercury or other metal alkyls may be produced at a rate faster than it is degraded by other organisms, it may accumulate in higher organisms such as fish. Hg species are also reduced to elementary Hg which is soluble in water but lost by volatilization to the atmosphere (40). 

Behavioral effects of OP insecticides have also been shown in birds (see review by Grue et al. 1991). Behavioral effects of OCs, OPs, and methylmercury on birds have been reviewed by Peakall (1985,1996). A remarkably wide range of behavioral tests were used in these studies. Tests employed included the following ... 

Methylmercury compounds at concentrations of 25.0 mg Hg/kg in soil were fatal to all tiger worms (Eisenia foetida) in 12 weeks at 5.0 mg/kg, however, only 21% died in a similar period (Beyer et al. 1985). Inorganic mercury compounds were also toxic to earthworms (Octochaetus pattoni) in 60 days, 50% died at soil Hg levels of 0.79 mg/kg, and all died at 5.0 mg/kg (Abbasi and Soni 1983). 

Most cases of mercury poisoning led to handicap, chronic disease, or death. The most frequent symptoms include numbness of limbs, lips and tongue, speech abnormalities, limb function disorders, visual acuity disorders, deafness, and muscular atrophy. Insomnia, hyperactivity, and coma have also been reported. Methylmercury penetrates the blood-brain barrier and causes central nervous system injuries. Mercury also has a teratogenic effect, leading to congenital abnormalities or congenital Minamata disease. 

Several recent epidemiological studies have involved examination of populations that consume unusually high levels of fish. One of these, conducted in the islands of the Seychelles, has not so far revealed behavioral and learning impairments in children whose mothers exhibited mercury levels (measured in hair) higher than those typically seen in the United States and European countries. But another study, conducted in the Faroe Islands, turned up evidence of cognitive and behavioral impairments in children. Scientists have struggled to understand why two well-done studies have produced such different outcomes, and some possible reasons have been suggested. The EPA and public health officials have acted on the basis of the Faroe data, out of both caution and also because they seem to be supported by other, more limited data, and by experimental studies. The debate is not so much about whether methylmercury is a developmental toxicant, but rather over the dose required. 

Two of the more interesting uses of pharmacokinetic data in risk assessment involve the neurotoxic agents lead and methylmercury (Chapter 4). In the case of lead, epidemiological studies have typically involved the development of quantitative relationships between levels of lead in the blood and adverse health effects. Other measures of lead in the body have also been used. Levels in blood are now very easy to measure, and they do carry the strong advantage that they integrate cumulative exposures from many possible sources (water, food, paint, soil, air, consumer products). Current public health targets for lead are expressed as blood concentrations, typically in pg/dL (Chapter 4). 

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