Effects of stock or purified diet on rat liver enzymes involved in the synthesis of dimethyl selenide.
Rats fed either a stock deit or a purified diet based on casein were tested for their ability to convert 75Se-sodium selenite to volatile selenium (dimethyl selenide) in vivo. This conversion was also studied in liver and kidney in vitro. When injected with a subacute dose of selenite (2 mg Se/kg), rats previously fed stock diet volatilized more than twice as much of the dose compared to rats fed the purified diet, confirming earlier findings. Parallel dietary effects were also observed in vitro using subcellular fractions incubated with 75Se-selenite, glutathione, TPNH, and S-adenosylmethionine. The 9-000 X g supernate prepared from rats fed stock diet synthesized dimethyl selenide at approximately twice the rate of that prepared from rats fed purified diet. A fourfold higher activity was observed with liver microsomal fractions from rats fed the stock diet, whereas cytosol was slightly more active in rats fed the purified diet. Kidney fractions showed analogous changes with diet, although the activity of kidney microsomal fraction was very low. Only minor differences in the levels of glutathione reductase, nonspecific disulfide reducatse, and non-protein thiols were observed in liver and kidney from rats fed the two diets. Considering the effects of diet on the various enzymes known from our previous studies to be involved in dimethyl selenide synthesis, it was concluded that the enhanced ability of rats fed stock diet to synthesize dimethyl selenide results from the induction of a liver microsomal enzyme, apparently a Se-methyltransferase, caused by unknown substances in the stock diet.
Effects of stock or purified diet on rat liver enzymes involved in the synthesis of dimethyl selenide. Rats fed either a stock deit or a purified diet based on casein were tested for their ability to convert 75Se-sodium selenite to volatile selenium (dimethyl selenide) in vivo. This conversion was also studied in liver and kidney in vitro. When injected with a subacute dose of selenite (2 mg Se/kg), rats previously fed stock diet volatilized more than twice as much of the dose compared to rats fed the purified diet, confirming earlier findings. Parallel dietary effects were also observed in vitro using subcellular fractions incubated with 75Se-selenite, glutathione, TPNH, and S-adenosylmethionine. The 9-000 X g supernate prepared from rats fed stock diet synthesized dimethyl selenide at approximately twice the rate of that prepared from rats fed purified diet. A fourfold higher activity was observed with liver microsomal fractions from rats fed the stock diet, whereas cytosol was slightly more active in rats fed the purified diet. Kidney fractions showed analogous changes with diet, although the activity of kidney microsomal fraction was very low. Only minor differences in the levels of glutathione reductase, nonspecific disulfide reducatse, and non-protein thiols were observed in liver and kidney from rats fed the two diets. Considering the effects of diet on the various enzymes known from our previous studies to be involved in dimethyl selenide synthesis, it was concluded that the enhanced ability of rats fed stock diet to synthesize dimethyl selenide results from the induction of a liver microsomal enzyme, apparently a Se-methyltransferase, caused by unknown substances in the stock diet.