Biological methylation of mercury

Landner L (1971) Biochemical model for biological methylation of mercury suggested from methylation studies in-vivo with Neurospora crassa. Nature 230 452-454. 

Berman, M. and R. Bartha. 1986. Levels of chemical versus biological methylation of mercury in sediments. Bull. Environ. Contam. Toxicol. 36 401-404. 

Jensen, S. and Jernelov, A., 1969. Biological methylation of mercury in aquatic organisms. Nature, 223 753—754. 

The biological methylation of mercury (e.g., from weathering, volcanism, fossil fuels, chloralkali electrolysis) is effected by microorganisms that utilize methylco-balamin (2c) see Section 5.1.2. 

Jensen, S., A. Jernelov, 1969, Biological Methylation of Mercury in Aquatic Organisms, Nature 223, pp. 753-754. 

It is now well established that organometallic compounds are formed in the environment from mercury, arsenic, selenium, tellurium and tin and hence were also deduced on the basis of analytical evidence for lead, germanium, antimony and thallium. Biological methylation of tin has been demonstrated by the use of experimental organisms. Methylgermanium and methyllead were widely found in the environment but it is debatable whether germanium and lead are directly methylated by biological activity in natural environment. 

Mercury dimethyl is a toxic environmental pollutant. It is found in polluted bottom sediments and in the bodies of fishes and birds. In the bodies of fishes and birds it occurs along with monomethyl mercury. The latter, as CH3Hg+ ion, is formed by microorganism-induced biological methylation of elemental mercury or agricultural fungicide mercury compounds that are discharged into the environment. 

In addition to manufactured organolead compounds, the possibility exists of biological meth-ylation of lead, such as occurs with mercury (see Section 12.7). However, there is a great deal of uncertainty regarding biological methylation of lead in the environment. 

The major complicating factor in environmental biogeochemistry of mercury and its speciation is the biological methylation of Hg " " to CHjHg" and (CH3)2Hg. This process converts inorganic mercury to organo-mercury, which is both more lipophilic and toxic (see below). 

The biological half-life in humans for methyl mercury is about 70 days because elimination is slow, irregular, and individualized, there is a considerable risk of an accumulation of mercury to toxic levels. A precise relationship between atmospheric levels of alkyl mercury and concentrations of mercury in blood or urine has not been shown. Clinical observations indicate that concentrations of 50-100pg mercury/lOOml of whole blood may be associated with symptoms of intoxication concentrations around 10-20pg mercury/ 100 ml are not associated with symptoms. In a study of 20 workers engaged in the manufacture of organic mercurials and exposed for 6 years to mercury concentrations in air between 0.01 and O.lmg/m, there was no evidence of physical impairment or clinical laboratory abnormalities. Low levels of methyl mercury in the blood do not seem to affect the results of behavioral performance tests. ... 

In spite of these limitations it is possible to obtain valuable data provided specific questions are posed. For example, it has been suggested that the level of methyl-mercury in a sample is a good indicator of the level of mercury toxicity Therefore it will be most useful to detect and quantify this species rather than to use the available resources to detect a wide range of mercury species, whose biological behaviour are yet to be established. It is essential to clearly define the purpose and use to which the information will be put before any speciation experiments are performed. This helps not only in the choice of the appropriate techniques and methods, but also helps to focus attention on the parameters that are useful for the interpretation of the results. 

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