TISSUE SELENIUM LEVELS AND GROWTH RESPONSES OF MICE FED SELENOMETHIONINE, SE-METHYLSELENOCYSTEINE OR SODIUM SELENITE

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Abstract
Mice fed diets containing selenomethionine at a level of 20 ppm selenium and raised to 30 ppm selenium at 3 weeks on experiment showed (1) delayed response to selenium toxicity, (2) slow recovery from the toxicity after removal of selenium from the diet and (3) relatively high deposition and retention of tissue selenium. These data suggest that selenomethonine initially becomes incorporated in to the primary structure of proteins and as such is not particularly toxic. However, upon its slow removal from protein, selenomethionine becomes toxic by forming selenium IV compounds through a pathway similar to that followed by methionine. Mice fed diets containing sodium selenite or Se-methylselenocysteine at the same level of selenium as the selenomethionine diet showed (1) immediate response to selenium toxicity (2) rapid recovery from the toxicity after removal of selenium from the diet and (3) relatively low deposition and relatively rapid depletion of tissue selenium. These data suggest that sodium selenite and Se-methylselenocysteine ultimately follow similar metabolic pathways and do not become part of the primary structure of proteins. A possible metabolic route for Se-methylselenocysteine is that it is oxidized to toxic selenium IV compounds through an oxidative pathway similar to that followed by S-methylcysteine.