It is well established that the toxicity of silver and methylmercury is suppressed by the presence of low levels of vitamin E or selenium in the diet, but little is known of the mechanisms involved. Silver induces a conditioned deficiency of selenium in rats, as shown by its effects on tissue levels of selenium and glutathione peroxidase (a selenoprotein), but methylmercury does not. Supplements of selenium do not decrease mercury levels in tissues of animals given methylmercury, and animals given selenium plus methylmercury may accumulate high levels of mercury without signs of toxicity. Although an equimolar accumulation of selenium and mercury in tissues sometimes occurs and could lead to mutual detoxification, such a coaccumulation is not always linked to protection. The only known functions of vitamin E and selenium are related to the prevention of oxidative damage. It is possible that their protective effects against heavy metals may involve such functions, thus accounting for the protection afforded by low levels of the nutrients against high levels of the metal toxicants.