Methylmercury mechanism

The mechanism through which a-methylmercury substituents eliminate Wolff rearrangements of acyl- and carboalkoxymethylenes is not clearly evident. 

Munthe, J., H. Hultberg, and A. Ivefeldt. 1995. Mechanisms of deposition of methylmercury and mercury to coniferous forests. Water Air Soil Pollut. 80 363-371. 

This is confusing. Why don t risk assessors simply decide what level of exposure is safe for each chemical, and risk managers simply put into effect mechanisms to ensure that industry reaches the safe level Why should different sources of risk be treated differently Why apply a no risk standard to certain substances (e.g., those intentionally introduced into food, such as aspartame) and an apparently more lenient risk-henefit standard to unwanted contaminants of food such as PCBs, methylmercury, and aflatoxins (which the FDA applies under another section of food law) Why allow technological limitations to influence any decision about health What is this risk-henefit balancing nonsense Aren t some of these statutes simply sophisticated mechanisms to allow polluters to expose people to risk ... 

Other Mechanisms. We acknowledge that numerous other processes (such as detritivore activity and microbial transformations) may affect transport across the interface, but our techniques could evaluate only the processes previously discussed. An obvious area for future research is microbial degradation and release of methylmercury from sediments. The assessment of factors regulating this transformation and release is essential for predictive models on Hg transport and bioaccumulation. 

The observation that victims of the Japanese Minamata disaster had suffered considerable damage to plasma membranes has led to investigation of possible reaction mechanisms whereby such damage may result from MeHg+ poisoning. It has been demonstrated that methylmercury is the most potent inhibitor of the enzyme adenyl cyclase yet reported.284 The enzyme occurs in liver plasma membranes and plays a part in the metabolism of mammalian cells. 

Cellular and molecular mechanisms of neurotoxicity are also influenced by the fact that neurons are postmitotic and do not divide. Thus, the capacity for replacement of damaged cells does not exist in the nervous system, whereas most other organ systems have a well-established capacity for regeneration. Many neurotoxins can cause encephalopathy and an important concept in neurotoxicology is the delayed manifestation of symptoms sometimes up to years after the exposure started. Several agents show a lag time between exposure and neurotoxicity. Examples are the organophosphate chemical warfare agents [245], bismuth intoxications [246] and methylmercury... 

Methylmercury and trimethyltin also produce neuronopathies. Methylmercury inhibits protein synthesis, but experimental evidence suggests that additional or alternative mechanisms must exist to account for the neuronal degeneration. The mechanism of action of trimethyltin is unknown. 

The methylmercury tragedy and the role of vitamin have generated much current research as well. Pratt has reviewed the extensive chemistry of the latter 213, 214). Methylcobalamin s role in methylation likewise received attention (2, 3, 20, 206). The myriad aspects of the mechanism by which methylmercuric compounds and other organomercurials interact with biochemical processes are being studied by many groups of professionals. 

Not much is known about the toxic effects of ethylmercury and most toxicologists have assumed that the toxic changes would be similar to that caused by methylmercury. These alterations in turn are very complex and depend on duration of exposure, dose, and the age of the individual. Mercury salts have a strong affinity for sulfhydryl groups and this is likely to play a role in effecting their neurotoxicity. Some in vitro studies indicate that oxidative stress leading to lipid peroxidation and DNA damage may also underlie the mechanism of toxicity. 

In the environment, inorganic mercury can be methylated by microorganisms to methylmercury. Methyl-mercury will accumulate in the tissues of organisms. The animals at the top of the food chain tend to accumulate the most methylmercury in their bodies. Any source of mercury release to the environment may, therefore, lead to increased levels of methylmercury in tissues of large fish and mammals. Occupational exposures are primarily to metallic mercury vapor. Accidental exposures to mercury are more common than accidental exposures to many hazardous substances, because liquid mercury is shiny and interesting, and because liquid mercury has been used in many electrical and mechanical devices. Accidental exposures, even to small amounts of mercury, may be harmful. Liquid mercury is poorly absorbed by the skin and from the intestines, but vapors that are released from liquid mercury are readily absorbed through the lungs and are very harmful when inhaled. The text in this chapter provides considerable detail on a number of accidental exposures to all forms of mercury. This information is intended to inform the reader and help prevent accidental exposures in the future. 

In summary, methylmercury is neurotoxic to humans and to several species of experimental animals following acute, intermediate, and chronic oral exposure. The major effects that are seen across the studies include motor disturbances, such as ataxia and tremors, as well as signs of sensory dysfunction, such as impaired vision. The predominant neuropathological feature is degenerative changes in the cerebellum, which is likely to be the mechanism involved in many of the motor dysfunctions. In humans, disruptions of higher functions have also been noted, as evidenced by depression and irritability. 

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