Elemental mercury excretion

Unithiol and succimer increase urine mercury excretion following acute or chronic elemental mercury inhalation, but the impact of such treatment on clinical outcome is unknown. Dimercaprol has been shown to redistribute mercury to the central nervous system from other tissue sites, and since the brain is a key target organ, dimercaprol should not be used in treatment of exposure to elemental or organic mercury. Limited data suggest that succimer, unithiol, and N- acetyl-L-cysteine (NAC) may enhance body clearance of methylmercury. 

Dimercaprol is FDA-approved as single-agent treatment of acute poisoning by arsenic and inorganic or elemental mercury and for the treatment of severe lead poisoning when used in conjunction with edetate calcium disodium (EDTA see below). Although studies of its metabolism in humans are limited, intramuscularly administered dimercaprol appears to be readily absorbed, metabolized, and excreted by the kidney within 4-8 hours. Animal models indicate that it may also undergo biliary excretion, but the role of this excretory route in humans and other details of its biotransformation are uncertain. 

Metallic (elemental) mercury. In acute or chronic poisoning, oral suc-cimer (DMSA, p 501) or oral unithiol (DMPS, p 506) may enhance urinary Hg excretion (although its effect on clinical outcome has not been fully studied). Although penicillamine (p 484) Is an alternative oral treatment. It may be associated with more side effects and less efficient Hg excretion. 

Clarkson TW, Magos C, Greenwood MR (1972) The transport of elemental mercury into fetal tissues. Biol. Neonat. (Basel) 21 239 Clarkson TW, Gatzy J, Dalton C (1961) Studies on the equilibration of mercury vapor with blood. Division of Radiation Chemistry and Toxicology, Univ. of Rochester Atom. Ener. Proj., Rochester, New York, UR-582 Clarkson TW, Rothstein A (1964) The excretion of volatile mercury by rats injected with mercuric salts. Health Phys. 10 1115... 

The half-lives of toxic metals vary over an enormous range and the value for a given toxic metal depends upon the site at which it is deposited. Thus the half-life of mercury in the whole blood of men following exposure to mercury vapor was found to be 3.1 days for a fast phase and 18 days for a slow phase. In this same study the half-life for the mercury in the urine was found to be 40 days (Barregard et al. 1992). In a similar study of a more severe human exposure a half-life of 45 days was estimated (Bluhm et al. 1992). In this latter group of workers the administration of DMSA produced a threefold increase in the amount of mercury excreted in the urine, while the administration of A-acetyl-D,L-penicillamine produced a twofold increase. The half-life of mercury in the human brain may be much longer than this (Cavanagh 1988). The half-life of elements which deposit in the bone, such as lead, can be of the order of many years (Rabinowitz et al. 1976). 

Bhattacharyya MH, Peterson DP (1979) Action of DTPA on hepatic plutonium. III. Evidence for a direct chelation mechanism for DTPA-induced excretion of monomeric plutonium into rat bile. Radiat Res 80 108-115 Bluhm RE, Bobbit RG, Welch LW, Wood AJJ, Bonfiglio JF, Sarzen C, Heath AJ, Branch RA (1992) Elemental mercury vapour toxicity, treatment, and prognosis after acute, intensive exposure in chloralkali plant workers. I. History, neuropsychological findings and chelator effects. Hum Exp Toxicol 11 201-210 Buchet JP, Lauwerys RR (1989) Influence of 2,3 dimercaptopropane-1-sulfonate and dimercaptosuccinic acid on the mobilization of mercury from tissues of rats pretreated with mercuric chloride, phenylmercury acetate or mercury vapors. Toxicology 54 323-333... 

Not all agents can be readily metabolized. The toxic metals lead and mercury are elements that cannot be degraded but must still be removed from the body. Another important mechanism of detoxification is the attachment or binding of another compound to a toxic chemical to make it easier for the kidney to filter the compound out of the blood and excrete it in the urine. A primary purpose of the kidney is to screen the blood for waste products and concentrate them in the urine for excretion, as occurs, for example, with mercury. Caffeine is excreted in the urine at approximately the same concentration as the blood because the kidney cannot concentrate caffeine. Vitamins, however, are readily concentrated and excess quickly eliminated in the urine. 

Nixon DE, Burrit ME and Moyer TP (1999) The determination of mercury in whole blood and urine by inductively coupled plasma mass spectrometry. Spectrochim Acta Part B 54 1141-1153. Nordenhall K, Dock L and Vahter M (1998) Cross-fostering study of methyl mercury retention, demethylation and excretion in the neonatal hamster. Pharmacol Toxicol 82 132-136. Novozamsky 1, Van der Lee HJ and Houba VJG (1995) Sample digestion proceduresfor trace element determination. Mikrochim Acta 119 183 — 189. NRC National Research Council, Committee ON Toxicological Effects of Methylmercury... 

A. Specific levels. Elemental and inorganic mercury follow a biphasic elimination rate (initially rapid, then slow), and both urinary and fecal excretion occur. The urinary elimination half-life is approximately 40 days. 

Depending on the form and concentration of mercury, the routes of exposure (such as inhalation, ingestion or dermal contact), the levels of exposure and the toxicokinetic mechanisms (i.e. absorption, distribution, metabolism and excretion), mercury can be very dangerous element with severe health effects in both aquatic and teiTestrial ecosystems. The combination of the above mentioned mechanisms and conditions with the different chemical foims of mercury will determine the risk associated to humans, ecosystems and wildlife. 

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