Biological Trace Element Research

, Volume 119, Issue 3, pp 255–268

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

Authors

    • Energy and Environmental Research CenterUniversity of North Dakota
  • J. Lloyd BlackwellIII
    • Department of EconomicsUniversity of North Dakota
  • Laura J. Raymond
    • Energy and Environmental Research CenterUniversity of North Dakota
Article

DOI: 10.1007/s12011-007-8005-7

Cite this article as:
Ralston, N.V.C., Blackwell, J.L. & Raymond, L.J. Biol Trace Elem Res (2007) 119: 255. doi:10.1007/s12011-007-8005-7

Abstract

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 μmol/kg, respectively) These diets were prepared with no added methylmercury (MeHg) or with moderate- or high-MeHg (0.2, 10 or 60 μmol/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.

Keywords

SeleniumMercuryMethylmercuryToxicityBrainBlood

Copyright information

© Humana Press Inc. 2007