Excretion mercury

Selenium lessens the toxicity of divalent mercury in animals, the protection being less at continuous mercury exposure. Selenium has been found to affect the distribution of mercuric mercury in mice [134], rats [135], rabbits [136, 137] and pigs [ 138]. Mercury forms a mercury-selenium protein complex with selenium with little biological activity [139]. Mercury is thus retained longer in the blood, liver and spleen and as a consequence lessens accumulation in the kidney. In fish, selenium pretreatment probably retarded mercury uptake rather than promoting mercury excretion [140]. 

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. 

Torres-Alanis O, Garza-Ocanas L, Pineyro-Lopez A. Evaluation of urinary mercury excretion after administration of 2,3-dimercapto-l-propane sulfonic acid to occupationally exposed men. J Toxicol Clin Toxicol l995 33(6) 7l7-20. 

Morcillo and Santamaria (1995) report absorption of 30-40% for radiolabeled mercuric chloride when administered in drinking water at 5, 50, and 500 M Hg for 8 weeks to male rats. The percentage of total mercury excreted by the fecal route was significantly lower in the 500 compared to the 5 and 50 M Hg... 

Data are limited on elimination of metallic and inorganic mercury in animals. Initial excretion of mercury is predominantly in the fecal matter following inhalation of metallic mercury vapor, but as mercury concentrations increase in the kidneys, urinary excretion increases (Rothstein and Hayes 1964). After inhalation, approximately 10-20% of the total excreted metallic mercury is by exhalation (Rothstein and Hayes 1964). Mercury is excreted in the urine of mice exposed orally to mercuric sulfide ( 8-200 mg Hg/kg) (Yeoh et al. 1986, 1989). The amount of mercury in the urine of the treated group was 4.5-15-fold greater than the control levels. Urinary rates of mercury excretion were 1.6-2.2 ng/hour. Neonatal rats (1, 8, and 15 days old) eliminated mercury slower than older rats (22 and 29 days old) given mercuric chloride subcutaneously (Daston et al. 1986). 

Organic Mercury. The fecal (biliary) pathway is the predominant excretory route for methylmercury, with less than one-third of the total mercury excretion occurring through the urine, following oral and inhalation exposure (Norseth and Clarkson 1970). In humans, nearly all of the total mercury in the feces after organic mercury administration is in the inorganic form. The conversion of methylmercury to inorganic mercury is a major step that is dependent on the duration of exposure and/or the duration after cessation of exposure. 

The rate of mercury excretion was also slower in younger animals (7 or 15 days) than in older animals (24 and 56 days) (Thomas et al. 1982). This age-dependent difference in the rate of mercury excretion may reflect differences in the sites of mercury deposition (i. e., hair, red blood cells, skin). In neonatal rats, the excretion of methylmercury is longer than in adult rats because of the inability of the neonatal liver to secrete the toxicant into the bile. Therefore, the immaturity of the transport system in neonatal rats affects the elimination of mercury. 

An association between urine mercury levels and performance on memory tests and verbal intelligence tests has been established. Abnormal results on memory tests were reported for 9 workers exposed to mercury in the production of thermometers urinary mercury excretion levels were 7-1,101 g/24 hours (Vroom and Greer 1972). The short-term memory span of 26 workers was examined by Smith et al. (1983) and found to decrease with increasing urine mercury levels. The range of mercury found in the urine of these workers was 0-510 g/L. A significant linear relationship was reported between subjects 50% memory threshold spans and 12-month urinary mercury concentrations. Disturbances on tests of verbal intelligence and memory were more frequent among individuals with mercury blood levels above 1.5 g/100 mL and mercury urine levels above 56 g/L in 36 male chloralkali workers (Piikivi et al. 1984). 

DMPS and DMSA are derivatives of BAL, but they have been found to be more effective than BAL in experimental studies. Although still considered an investigational drug, DMPS decreased the mercury excretion half-life from 33.1 to 11.2 days in 2 workers exposed to high levels of mercury vapor (ATSDR 1992). In a study of the influence of DMPS and DMSA on renal deposition of mercury in rats, both... 

Bell ZG, Lovejoy HB, Vizena TR. 1973. Mercury exposure evaluations and their correlations with urine mercury excretion 3. Time-weighted average (TWA) mercury exposures and urine mercury levels. 

Lovejoy HB, Bell ZG, Vizena TR. 1974. Mercury exposure evaluations and their correlation with urine mercury excretion. J Occup Med 15 590-591. 

Nakamura I, Hosokawa K, Tamra H, et al. 1977. Reduced mercury excretion with feces in germffee mice after oral administration of methylmercury chloride. Bull Environ Contain Toxicol 17 528-533. 

Stewart W, Guirgis H, Sanderson J, et al. 1977. Urinary mercury excretion and proteinuria in pathology laboratory staff. Br J Ind Med 34 26-31. 

Landry, T.D., R. A. Doherty, and A.H. Gates. 1979. Effects of three diets on mercury excretion after methylmercury administration. Bull. Environ. Contam. Toxicol. 22(1-2) 151-158. 

Human volunteers exhaled approximately 7-12% of a retained dose of mercury vapor within the first few days after exposure (Hursh etal. 1976, Sandborgh-Englund etal. 1998). Under normal circumstances, the excretion of Hg" " via sweat is negligible, but in the case of acute mercury vapor inhalation at toxic dosage, the proportion of mercury excreted in the sweat was of similar magnitude to that excreted renally (Lovejoy etal. 1973, EPA 1997). 

B. Succimer is protective against the acute lethal and nephrotoxic effects of mercuric salts in animal models, and increases urinary mercury excretion in animals and humans. It may therefore have clinical utility in the treatment of human poisoning by inorganic mercury. 

Levy M, Schwartz S, Dijak M, Weber JP, Tardif R, Rouah F (2004) ChUdhood urine mercury excretion dental amalgam and fish consumption as exposure factors. Environ Res 94 283-290... 

Woods JS, Martin MD, Leroux BG, DeRouen TA, Leitao JG, Bernardo MF, Luis HS, Simmonds PL, Kushleika JV, Huang Y (2007) The contribution of dental amalgam to urinary mercury excretion in children. Environ Health Perspect 115 1527-1531 World Health Organization (WHO) (1990) Intemationrd program on chemical safety. Environmental Health Criteria 101, Rome... 

Cd and 203gg absorption in suckling rats. Environ. Res 25 281-285 Landry TD, Doherty RA, Gates AH (1979) Effects of three diets on mercury excretion after methylmercury administration. Bull. Environ. Contam. Toxicol 22 151-158 Lecce JG (1972) Selective absorption of macromolecules into intestinal epithelium and blood by neonatal mice. J.. Nutr 102 69-75 McCabe EB (1979) Age and sensitivity to lead toxicity A review. Environ. Health Perspect 29 29-33... 

The mechanism of mercury excretion in the bile is unknown. Binding to glutathione and cysteine has been demonstrated in rodents (Refsvik and Norseth, 1975). The excretion through the intestinal mucosa may be related to the plasma protein turnover. The relative importance of the main excretory routes - by feces and by urine - is dose-dependent -with higher doses, a larger portion is excreted by urine (Lomholt, 1928). 

A certain elimination of methyl mercury may occur in other parts in the intestinal canal and may possibly be linked with the plasma protein turnover in the intestinal tract. An important factor in the excretion by the fecal route is the enterohepatic circulation of methyl mercury. Methyl mercury excreted into the bile or through the intestinal mucosa is likely to be reabsorbed unless it is decomposed in the gut to inorganic mercury, which has been proven to occur due to the microbiological activity in the gut of the mouse (Nakamura et al., 1977), the rat and man (Rowland et al., 1977). 

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