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Human red blood cell uptake and sequestration of arsenite and selenite: Evidence of seleno-bis(S-glutathionyl) arsinium ion formation in human cells. | LitMetric

Human red blood cell uptake and sequestration of arsenite and selenite: Evidence of seleno-bis(S-glutathionyl) arsinium ion formation in human cells.

Biochem Pharmacol

Division of Analytical and Environmental Toxicology, Department of Laboratory Medicine and Pathology, University of Alberta, Canada; Membrane Protein Disease Research Group, University of Alberta, Canada; Department of Physiology, University of Alberta, Canada. Electronic address:

Published: October 2020

AI Article Synopsis

  • Over 200 million people are at risk from drinking water contaminated with arsenic, a known human carcinogen, and the interaction between arsenic and selenium in human red blood cells (RBCs) poses potential health implications.
  • The study investigates how human RBCs absorb arsenite (As) and selenite (Se), examining whether they influence each other's accumulation through a complex called [(GS)AsSe], which could help detoxify these compounds.
  • Findings suggest that both As and Se enhance each other's uptake in RBCs, and the formation of [(GS)AsSe] may help to mitigate arsenic's harmful effects by slowing its distribution in the body.

Article Abstract

Over 200 million people worldwide are exposed to the human carcinogen, arsenic, in contaminated drinking water. In laboratory animals, arsenic and the essential trace element, selenium, can undergo mutual detoxification through the formation of the seleno-bis(S-glutathionyl) arsinium ion [(GS)AsSe], which undergoes biliary and fecal elimination. [(GS)AsSe], formed in animal red blood cells (RBCs), sequesters arsenic and selenium, and slows the distribution of both compounds to peripheral tissues susceptible to toxic effects. In human RBCs, the influence of arsenic on selenium accumulation, and vice versa, is largely unknown. The study aims were to characterize arsenite (As) and selenite (Se) uptake by human RBCs, to determine if Se and As increase the respective accumulation of the other in human RBCs, and ultimately to determine if this occurs through the formation and sequestration of [(GS)AsSe]. Se accumulation was temperature and Cl-dependent, inhibited by 4,4'-diisothiocyanatodihydrostilbene-2,2'-disulfonic acid (HDIDS) (IC 1 ± 0.2 µM), and approached saturation at 30 µM, suggesting uptake is mediated by the erythrocyte anion-exchanger 1 (AE1 or Band 3, gene SLC4A1). HEK293 cells overexpressing AE1 showed concentration-dependent Se uptake. As uptake by human RBCs was temperature-dependent, partly reduced by aquaglyceroporin 3 inhibitors, and not saturated. As increased Se accumulation (in the presence of albumin) and Se increased As accumulation in human RBCs. Near-edge X-ray absorption spectroscopy revealed the formation of [(GS)AsSe] in human RBCs exposed to both As and Se. The sequestration of [(GS)AsSe] in human RBCs potentially slows arsenic distribution to susceptible tissues and could reduce arsenic-induced disease.

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Source
http://dx.doi.org/10.1016/j.bcp.2020.114141DOI Listing

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