Cited by 233Erythrocyte Function and PathophysiologyRedox biology and oxidative stressIon Transport and Channel Regulation

Oxidation induces a Cl−‐dependent cation conductance in human red blood cells

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Duranton, Christophe, Huber, Stephan M., Lang, Florian·2002·The Journal of Physiology

Abstract

Oxidative stress induces complex alterations of membrane proteins in red blood cells (RBCs) eventually leading to haemolysis. To study changes of membrane ion permeability induced by oxidative stress, whole‐cell patch‐clamp recordings and haemolysis experiments were performed in control and oxidised human RBCs. Control RBCs exhibited a small cation‐selective whole‐cell conductance (236 ± 38 pS; n= 8) which was highly sensitive to the external Cl− concentration: replacement of NaCl in the bath by sodium gluconate induced an increase of this cation conductance by about 85 %. Exposing RBCs to t‐butylhydroxyperoxide (1 m m for 10 min) induced a twofold increase in this cation conductance which was further stimulated after replacement of extracellular Cl− by gluconate, Br−, I− or SCN−. In addition, lowering the ionic strength of the bath solution by isosmotic substitution of NaCl by sorbitol activated the cation conductance. The Cl−‐sensitive and oxidation‐induced cation conductance was Ca 2+ permeable, exhibited a permselectivity of Cs+ > K+ > Na+= Li+ >> NMDG+, and was partially inhibited by amiloride (1 m m) and almost completely inhibited by GdCl 3 (150 μ m), but was insensitive to TEA, BaCl 2, NPPB, flufenamic acid or quinidine. DIDS (100 μ m) reversibly inhibited the activation of the cation conductance by removal of external Cl−. Oxidation induced haemolysis in NaCl‐bathed human RBCs. This haemolysis was attenuated by amiloride (1 m m) and inhibited by replacement of bath Na+ by the impermeant cation NMDG+. The Na+‐ and Ca 2+‐permeable conductance might be involved in haemolytic diseases induced by elevated oxidative stress, such as glucose‐6‐phosphate dehydrogenase deficiency.

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Crossref · 10.1113/jphysiol.2001.013040

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Authors
Duranton, C., Huber, S. M., & Lang, F.
Affiliations
University of Tübingen (DE)
Corresponding author
Duranton, Christophe
Venue
The Journal of Physiology
Publisher
Wiley
Published
2002-03
Volume
539
Issue
3
Pages
847-855
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
OpenAlex
W2039659095
Cited by
233
References
25
Citations by year
2026: 1 · 2025: 2 · 2024: 3 · 2023: 8 · 2022: 4 · 2021: 5 · 2020: 3 · 2019: 6 · 2018: 3 · 2017: 2 · 2016: 4 · 2015: 4 · 2014: 7 · 2013: 10 · 2012: 10
FWCI
9.19
Type
journal article
Language
en
Open access
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Erythrocyte Function and Pathophysiology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
oxidative stress, human erythrocytes, cation conductance, hemolysis, membrane ion permeability, calcium permeability, amiloride, gadolinium, DIDS, glucose-6-phosphate dehydrogenase deficiency, hemolytic disease, ionic strength
MeSH terms
Cations, Chlorides, Electric Conductivity, Erythrocytes, Hemolysis, Humans, Ion Channels, Osmolar Concentration, Oxidation-Reduction, Permeability, Reference Values, Patch-Clamp Techniques

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