A study published in the June issue of Environmental Health Perspectives indicates that some genes have variations influencing the metabolism of methylmercury. These genes control a compound in the body called glutathione. Glutathione binds to methylmercury and brings it to the liver, where it can be excreted with bile.
Exposure to toxic methylmercury (MeHg) mainly through fish consumption is a large problem worldwide, and it has led to governmental recommendations for reducing fish consumption and blacklisting of highly contaminated fish (see EVISA's news section below). Risk assessment for different populations is complicated by the fact that elimination kinetics of MeHg varies greatly among individuals. The elimination half-time of MeHg varies greatly among individuals, ranging from 45 to 70 days (Clarkson 2002), but extreme values, up to almost 190 days, have been reported (Al-Shahristani and Shihab 1974). One possible explanation is hereditary differences in MeHg metabolism. MeHg is eliminated from the body as a glutathione (GSH) conjugate.The new study:
The Swedish research group conducted this study to assess the influence of polymorphisms in GSH-synthesizing genes on MeHg retention. They measured total Hg in erythrocytes (Ery-Hg) and long-chain n-3 polyunsaturated fatty acids in plasma (P-PUFA; an exposure marker for fish intake) from 292 subjects from northern Sweden that had a high consumption of fish (lean/fat fish two to three times per week or more).
Results of the present study indicate that polymorphisms in GCLM and GST genes modify the relationship between exposure to and retention of MeHg. Two polymorphisms in GSTP1 modified the Ery-Hg levels at high MeHg
exposures, whereas homozygotes for the GCLM-588 polymorphism had higher Ery-Hg levels but showed no evidence of effect modification.
Another outcome of the study was the rise of Ery-Hg with increasing age. Increasing age may also be associated with impairment of the metabolism of MeHg. Indeed, both GSH and GST levels have been shown to decrease with age (Voss and Siems 2006).
The researchers concluded their report by stressing the importance of information on genetic impact on MeHg metabolism, because it may mean a difference in susceptibility to toxic effects, which may influence the risk assessment and thus the foundation of preventive actions. The new study:
Karin Schläwicke Engström, Ulf Strömberg, Thomas Lundh, Ingegerd Johansson, Bengt Vessby, Göran Hallmans, Staffan Skerfving, Karin Broberg, Genetic Variation in Glutathione-Related Genes and Body Burden of Methylmercury
, Environ. Health Perspect., 116/6 (2008) 734-739. DOI: 10.1289/ehp.10804 Related studies:
H. Al-Shahristani, K.M. Shihab, Variation of biological half-life of methylmercury in man
, Arch. Environ. Health, 28 (1974) 342-344. DOI:
N. Ballatori, T.W. Clarkson, Biliary secretion of glutathione and of glutathione-metal complexes, Fundam. Appl. Toxicol., 5 (1985) 816-831. DOI: 10.1016/0272-0590(85)90165-4
W.J. Dutczak, N. Ballatori, Transport of the glutathione-methylmercury complex across liver canalicular membranes on reduced glutathione carriers,
J. Biol. Chem., 269 (1994) 9746-9751. PMID:
T.W. Clarkson, The three modern faces of mercury
, Environ. Health Perspect., 110/S.1 (2002) 11-23. DOI: 10.1289/ehp.02110s111
H.M. Custodio, K. Broberg, M. Wennberg, J.H. Jansson, B. Vessby, G. Hallmans, Polymorphisms in glutathione-related genes affect methylmercury retention, Arch. Environ. Health, 59 (2004) 588-595. DOI: 10.1080/00039890409603438 Related EVISA News (newest first)
last time modified: June 26, 2020