Silent latency periods in methylmercury poisoning and in neurodegenerative disease.

Weiss, Bernard; Clarkson, Thomas W.; Simon, William J.

doi:10.1289/ehp.02110s5851

Cited by 181 publications

(113 citation statements)

References 17 publications

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“…It has been proposed that latency period associated with MeHg exposure might be due to the slow production and accumulation of the divalent inorganic mercury in the brain over periods of months . However, as reported by Weiss et al (2002) one would expect the buildup of inorganic mercury to be faster at higher levels of MeHg exposure, resulting in a shorter latency period. This is contrary to evidence published in the literature (Magos et al 1985;Weiss et al 2002).…”

Section: Because Ethylmercury Decomposes Much Faster Than Mehg the Rmentioning

confidence: 68%

Are Neuropathological Conditions Relevant to Ethylmercury Exposure?

Aschner

Ceccatelli

2009

Neurotox Res

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Mercury and mercurial compounds are among the environmentally ubiquitous substances most toxic to both wildlife and humans. Once released into the environment from both natural and anthropogenic sources, mercury exists mainly as three different molecular species: elemental, inorganic, and organic. Potential health risks have been reported from exposure to all forms; however, of particular concern for human exposure relate to the potent neurotoxic effects of methylmercury (MeHg), especially for the developing nervous system. The general population is primarily exposed to MeHg by seafood consumption. In addition, some pharmaceuticals, including vaccines, have been, and some continue to be, a ubiquitous source of exposure to mercurials. A significant controversy has been whether the vaccine preservative ethylmercury thiosalicylate, commonly known as thimerosal, could cause the development of autism. In this review, we have discussed the hypothesis that exposure to thimerosal during childhood may be a primary cause of autism. The conclusion is that there are no reliable data indicating that administration of vaccines containing thimerosal is a primary cause of autism. However, one cannot rule out the possibility that the individual gene profile and/or gene-environment interactions may play a role in modulating the response to acquired risk by modifying the individual susceptibility.

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Section: Because Ethylmercury Decomposes Much Faster Than Mehg the Rmentioning

confidence: 68%

Are Neuropathological Conditions Relevant to Ethylmercury Exposure?

Aschner

Ceccatelli

2009

Neurotox Res

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“…As many of the selenoenzymes are active in protection against or reversal of oxidative damage, it is not surprising that oxidative damage would occur if their presence and activities diminished as a result of MeHg exposure. As incorporated MeHg is gradually demethylated to release intracellular Hg 2+ that has high binding affinities for Se, the Se sequestration hypothesis may also provide an explanation for the latency period that often accompanies exposure to toxic amounts of MeHg [54]. This mechanism could also explain why MeHg exposure severely compromised selenoenzyme activities in tissues of neonatal experimental animals whose dams were fed low dietary Se, but not in tissues of neonates whose dams were fed Se-rich diets [10,55].…”

Section: Discussionmentioning

confidence: 99%

Importance of Molar Ratios in Selenium-Dependent Protection Against Methylmercury Toxicity

Ralston

Blackwell

Raymond

2007

Biol Trace Elem Res

162

155

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The influence of dietary selenium (Se) on mercury (Hg) toxicity was studied in weanling male Long Evans rats. Rats were fed AIN-93G-based low-Se torula yeast diets or diets augmented with sodium selenite to attain adequate- or rich-Se levels (0.1, 1.0 or 15 micromol/kg, respectively) These diets were prepared with no added methylmercury (MeHg) or with moderate- or high-MeHg (0.2, 10 or 60 micromol/kg, respectively). Health and weights were monitored weekly. By the end of the 9-week study, MeHg toxicity had impaired growth of rats fed high-MeHg, low-Se diets by approximately 24% (p < 0.05) compared to the controls. Growth of rats fed high-MeHg, adequate-Se diets was impaired by approximately 8% (p < 0.05) relative to their control group, but rats fed high-MeHg, rich-Se diets did not show any growth impairment. Low-MeHg exposure did not affect rat growth at any dietary Se level. Concentrations of Hg in hair and blood reflected dietary MeHg exposure, but Hg toxicity was more directly related to the Hg to Se ratios. Results support the hypothesis that Hg-dependent sequestration of Se is a primary mechanism of Hg toxicity. Therefore, Hg to Se molar ratios provide a more reliable and comprehensive criteria for evaluating risks associated with MeHg exposure.

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“…For example, fish consumption is beneficial to the prevention of cardiovascular diseases and Alzheimer disease; however, several reports have indicated that fish consumption was the major source of mercury exposure. [83][84][85][86] Mercury is present in three forms in the environment, including elemental or metallic mercury, inorganic mercury and organic mercury. The mercury compounds are generally used in dry-cell batteries, fluorescent bulbs, arc lamps, mirrors, and in the extraction of gold and silver from ores, thermometers, dental amalgam fillings and vaccine preserver.…”

Section: Mercurymentioning

confidence: 99%