Interaction of selenite and arsenite on erythrocytes uptake of each metalloid: Possible mechanism mediated by extracellularly generated selenium-arsenic complexes

Abstract

It has been demonstrated that selenium (Se) and arsenic (As) interact in living organisms. The elucidation of the interaction mechanisms of these toxic metalloids is believed to be of great importance for understanding their effects on humans and animals. The seleno-bis(S-glutathionyl) arsinium ion [(GS)₂AsSe]⁻ has been identified as the major As metabolite present in the bile of rabbits and rats co-treated with selenite (iSeIV) and arsenite (iAsIII). Selenide (HSe⁻), a reduced form of iSeIV, is a crucial component in the As-Se-GSH conjugate formation. This study aimed to shed light on HSe⁻ released from erythrocytes and propose a novel mechanism for the uptake of As and Se into erythrocytes via Se-As complexes, in addition to a previously reported mechanism for [(GS)₂AsSe]⁻ formation. Erythrocytes from rats that had been fed As-depleted rodent chow for at least 7 weeks after weaning were used in the experiments. iAsIII and/or iSeIV were added to the erythrocyte suspension (final 10%) and incubated at 37℃ for up to 180 min or 10 min. The uptake of both elements into the erythrocytes was assessed by measuring the attenuation of each element in the supernatant. HSe⁻ was detected by measuring the syn-(methyl,-methyl) bimane produced from the reaction of monochlorobimane with HSe⁻. We observed that iAsIII was slightly taken up by erythrocytes. Furthermore, iSeIV was rapidly taken up by erythrocytes. Simultaneous exposure to both iSeIV and iAsIII increased Se and As uptake by erythrocytes. In addition, a temporal delay occurred in the uptake of both compounds. In conclusion, our study revealed that HSe⁻ release is more pronounced in selenite-treated erythrocytes and successfully proposed a novel mechanism for Se and As uptake.

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