The toxicity of most trace minerals is well understood and mechanisms are well documented in academic papers. Because selenium can accumulate in body proteins there is the potential for toxicity and this has been extensively studied in animal models. The median lethal dose (LD50) for selenomethionine is 4.25mg and 8.8 mg of selenium per kg of body weight, in rats and mice respectively. Selenomethionine shows a lower chronic toxicity that inorganic forms of selenium (such as selenate and selenite). In monkeys, the highest tolerable dose of selenomthionine is 150 µg of selenium per kg per day. Differences are present between the forms of selenium with regard the structural isomerism shown by the methionine part of the selenomethionine molecule. For humans, L-selenomethionine appears to be safer than the DL- and D- forms of the molecule.
Because selenomethionine is incorporated into body proteins, it is suggested that rapid breakdown of this protein might cause selenium toxicity. However, there is no mechanism known that would selectively release selenium from body proteins in this fashion. In addition, selenium toxicity is prevented from occurring by build up in tissues, because a steady state of accumulation and breakdown is established. Intakes of selenium are dependent on the source of the food because selenium in crops is dependent of soil levels. For this reason meat can be a more reliable source of selenium. Selenium intakes as high as 724 µg per day have been recorded in individuals taking supplements or living in high selenium soil areas. The reference dose for selenium in America (350 µg/day of selenium) has a wide margin of safety, and takes into account a selenium rich diet and a 200 µg selenium supplement.
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