To study the effects of long-term selenium supplementation on absorption, distribution, and elimination of methylmercury (MeHg) in mice, three groups of male mice (Balb/c CA) were exposed for 7 wk to 0, 0.6, and 3 ppm sodium selenite in tap water. They were then given a single oral dose of Me203Hg (2 mumol/kg) by gastric intubation, and elimination of 203Hg was followed by whole-body counting for 49 d at the same Se exposure as previously. Twenty-four hours and 49 d after dosage, 6-7 animals/group were sampled for analysis of 203Hg distribution in the body. Glutathione peroxidase (GSH-PX) activity in blood and selenium levels in the liver were used as measures of selenium status. Gastrointestinal absorption of Me203Hg was not influenced by the Se status of the animals. Selenium supplementation of MeHg-exposed mice caused an enhanced whole-body elimination of Hg, but selenium-supplemented animals did not have lower Hg levels in the brain and kidney than nonsupplemented animals. The effect of selenium on the accumulation of Hg in the brain was dose-dependent, a high dose (3 ppm Se) causing a higher initial accumulation of Hg. The intracellular distribution of 203Hg in the liver and kidney was not affected by Se. The results indicate that selenium treatment of MeHg-exposed mice may have a positive effect on the health of the animals by decreasing the total body burden of MeHg.