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Studies of selenium and arsenic mutual protection in human HepG2 cells.

Author information

Affiliations

  • 1. Division of Analytical and Environmental Toxicology, Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Alberta, Canada; Membrane Protein Disease Research Group, University of Alberta, Edmonton, Alberta, Canada.
      Authors
    • Kaur G 1
    • Zhou JR 1
    (2 authors)
  • 2. Department of Geological Sciences, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
      Authors
    • Ponomarenko O 2
    • Dolgova NV 2
    (2 authors)
  • 3. Membrane Protein Disease Research Group, University of Alberta, Edmonton, Alberta, Canada; Department of Physiology, University of Alberta, Edmonton, Alberta, Canada.
      Authors
    • Swanlund DP 3
    (1 author)
  • 4. Department of Geological Sciences, University of Saskatchewan, Saskatoon, Saskatchewan, Canada; Department of Chemistry, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
      Authors
    • Summers KL 4
    • Pickering IJ 4
    • George GN 4
    (3 authors)
  • 5. Advanced Photon Source, Argonne National Laboratory, Argonne, Illinois, USA.
      Authors
    • Antipova O 5
    (1 author)
    • Show all (6)

ORCIDs linked to this article

Chemico-biological Interactions, 07 Jun 2020, 327:109162
https://doi.org/10.1016/j.cbi.2020.109162 PMID: 32524993 

Abstract 

Hundreds of millions of people worldwide are exposed to unacceptable levels of carcinogenic inorganic arsenic. Animal models have shown that selenium and arsenic are mutually protective through the formation and elimination of the seleno-bis(S-glutathionyl) arsinium ion [(GS)2AsSe]-. Consistent with this, human selenium deficiency in arsenic-endemic regions is associated with arsenic-induced disease, leading to the initiation of human selenium supplementation trials. In contrast to the protective effect observed in vivo, in vitro studies have suggested that selenite increases arsenite cellular retention and toxicity. This difference might be explained by the rapid conversion of selenite to selenide in vivo. In the current study, selenite did not protect the human hepatoma (HepG2) cell line against the toxicity of arsenite at equimolar concentrations, however selenide increased the IC50 by 2.3-fold. Cytotoxicity assays of arsenite + selenite and arsenite + selenide at different molar ratios revealed higher overall mutual antagonism of arsenite + selenide toxicity than arsenite + selenite. Despite this protective effect, in comparison to 75Se-selenite, HepG2 cells in suspension were at least 3-fold more efficient at accumulating selenium from reduced 75Se-selenide, and its accumulation was further increased by arsenite. X-ray fluorescence imaging of HepG2 cells also showed that arsenic accumulation, in the presence of selenide, was higher than in the presence of selenite. These results are consistent with a greater intracellular availability of selenide relative to selenite for protection against arsenite, and the formation and retention of a less toxic product, possibly [(GS)2AsSe]-.

Full text links 

Read article at publisher's site: https://doi.org/10.1016/j.cbi.2020.109162

Read article for free, from open access legal sources, via Unpaywall: http://manuscript.elsevier.com/S000927972030569X/pdf/S000927972030569X.pdfUnpaywall

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Funding 

Funders who supported this work.

Canadian Institutes of Health Research