摘要：The metabolism of 75Se-labeled SeO32− and its conversion by intact rat erythrocytes in vitro to a form which complexes with Cd and plasma proteins were studied. By utilizing both excess SeO32− and N-ethylmaleimide to lower erythrocyte reduced glutathione (GSH) concentrations, it was shown that the uptake and metabolism of SeO32− were GSH-dependent, the probable intermediate being glutathione selenotrisulfide (GSSeSG). Secondary release of selenium by rat erythrocytes had no relation to the erythrocyte transport of oxidized glutathione (GSSG). While fluoride depressed and chromate increased GSSG transport, chromate, a glutathione reductase inhibitor, decreased selenium release. This release appeared to be secondary to a reaction catalyzed by glutathione reductase. The similarity of I50 values for chromate's inhibition of glutathione reductase and for the inhibition of selenium release further suggested a relationship between these two events. H2Se or a similar product of GSSeSG reduction is proposed to be the active product of SeO32− metabolism by rat erythrocytes. By use of gel-filtration and ion-exchange methods it was noted that the incubation of H2Se with cadmium and plasma produced a Cd–Se complex indistinguishable from that produced by incubation of Cd, SeO32−, plasma, and erythrocytes in vitro , or that noted following the administration of Cd and SeO3 in vivo . A mechanism whereby the tissue distribution and toxicity of cadmium are altered by selenium is suggested. Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (609K), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References . 133 134 135 136
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