Mercury brain toxicity

Trasande, L., Landrigan, P.J., and Schechter, C. (2005) Public health and economic consequences of methyl mercury toxicity to the developing brain. Environmental Health Perspectives 113 590-596. http //www.ehponline.org/members/2005/7743/7743.pdf. Cited 19 January 2009. 

During long-term constant exposure (several months) to methyl mercury in food, there is a linear relationship between daily intake of methyl mercury and the concentration of mercury in blood. The mercury concentration in blood (pg/L) corresponds to the daily intake of methyl mercury (pg/ day) multiplied by 0.5-1. When exposure is continuous, the blood mercury concentration is proportional to the concentration in the brain, the critical organ for methyl mercury toxicity. Because of mercury s short half-life in the blood (2-4 days), evaluation of blood mercury is of limited clinical value if a substantial amount of time has passed since time of exposure [43]. 

In a case report of four patients who were exposed to ethyl mercury, toxicity was seen in the brain, spinal motor neurons, peripheral nerves, skeletal muscles, and myocardium. Several case studies of accidental occupational exposure have also been documented. The most common signs of ethylmercury toxicity are paraesthesia, dysarthria, and constriction of the visual field. However, none of the symptoms of ethylmercury toxicity are specific and death is a common outcome if exposure levels are high. 

Barron, DJ University of Rochester Rochester, NY Mercury toxicity and the blood-brain factor. NIDCR... 

Chemical speciation is especially critical when assessing mercury toxicity. Metallic mercury, because of its volatility, presents a hazard that seems to undergo repeated rediscovery. Its ability to seep into fissures in surfaces such as floors, from which it volatilizes, often leads to neglect of necessary precautions because it is not visible. Mercury vapor also reaches the brain far more readily than the ionic forms. Since the conversion of elemental mercury to mercuric ion by blood is a slow process compared to the time required for transport from lung to brain, and since elemental mercury seems to penetrate readily into brain,CNS tissue may contain ten times more mercury after vapor exposure than after a comparable intravenous dose of mercuric salt. The mercury is then retained in brain after oxidation because the... 

A knowledge of physiology and pharmacokinetics is needed (Fanis et al. 1993 Monteiro and Furness 2001). Levels of mercuiy normally vary among internal tissues, and the time to equilibrate within each tissue varies. For example, blood mercury levels normally reflect veiy recent exposure, while brain and liver levels reflect longer-term exposure. Tissue-specific mechanisms of detoxification and seqnestration, among other processes, must be understood to define the bioactive moiety in observed tissue bmdens before a clear expression of toxicity can be derived (Woodetal. 1997). 

Brain is a key tissue to analyze for mercury concentration because it is the site of MeHg toxicity. The neurotoxic effects of MeHg in adrrlt mammals inclnde ataxia, difficulty in locomotion neurasthenia, a generalized weakness impairment of hearing... 

Methylation of divalent inorganic mercury salt has been shown in vivo in rat intestine [61] and in vitro in human intestine [62], yet it is seldom followed by toxic effects. MeHg has been found in hen tissues [63 ] and probably in rat brain [64] after ingestion of divalent mercuric salts. 

Mercury dimethyl is a highly toxic substance by all routes of exposure. Several cases of human poisoning are well documented. (Patnaik, P. 1999. A Comprehensive Guide to the Hazardous Properties of Chemical Substances, 2nJohn Wiley Sons.) The compound can accumulate in the brain and blood of humans. Intake of small quantities can cause death. 

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