Journal
ACS CHEMICAL BIOLOGY
Volume 15, Issue 10, Pages 2673-2682Publisher
AMER CHEMICAL SOC
DOI: 10.1021/acschembio.0c00309
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Funding
- Science and Engineering Research Board (SERB), New Delhi [EMR/IISc-01/2016]
- SERB/DST [SB/S2/JCB-067/2015]
- IISc
- SERB
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Red blood cell death or erythrocyte apoptosis (eryptosis) is generally mediated by oxidative stress, energy depletion, heavy metals exposure, or xenobiotics. As erythrocytes are a major target for oxidative stress due to their primary function as O-2-carrying cells, they possess an efficient antioxidant defense system consisting of glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), and peroxiredoxin 2 (Prx2). The oxidative stress-mediated activation of the Ca2+-permeable cation channel results in Ca2+ entry into the cells and subsequent cell death. Herein, we describe for the first time that selenium compounds having intramolecular diselenide or selenenyl sulfide moieties can prevent the oxidative stress-induced eryptosis by exhibiting an unusual Prx2-like redox activity under conditions when the cellular Prx2 and CAT enzymes inhibited.
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