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Related Experiment Videos

Hypochlorous acid mobilizes cellular zinc.

H Fliss1, M Ménard, M Desai

  • 1Department of Physiology, Faculty of Medicine, University of Ottawa, Ont., Canada.

Canadian Journal of Physiology and Pharmacology
|November 1, 1991
PubMed
Summary

Hypochlorous acid (HOCl), a neutrophil oxidant, mobilizes zinc ions (Zn2+) in tissues during inflammation. This zinc mobilization may contribute to tissue injury, but dithiothreitol can chelate and potentially reverse it.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Pathology

Background:

  • Neutrophil-derived oxidants, like hypochlorous acid (HOCl), contribute to tissue damage at inflammatory sites.
  • Oxidant-induced metal ion mobilization is a potential mechanism underlying this tissue injury.

Purpose of the Study:

  • To investigate the capacity of hypochlorous acid (HOCl) to mobilize zinc ions (Zn2+) within target tissues.
  • To explore the potential role of Zn2+ mobilization in HOCl-induced tissue injury.

Main Methods:

  • Utilized arterial endothelial cell cultures and heart tissue sections.
  • Employed a Zn2+-specific fluorescent chelator, N-(6-methoxy-8-quinolyl)-p-toluenesulfonamide, to detect free Zn2+.
  • Exposed tissues to HOCl and subsequently treated with dithiothreitol (DTT), a metal chelator.

Main Results:

  • HOCl treatment significantly increased cellular fluorescence, indicating elevated free Zn2+ concentrations.
  • Dithiothreitol (DTT) treatment of HOCl-exposed tissues markedly reduced cellular fluorescence.
  • This study provides the first evidence of HOCl-induced mobilization of cellular Zn2+.

Conclusions:

  • Hypochlorous acid (HOCl) can mobilize intracellular zinc (Zn2+) in biological tissues.
  • Mobilization of Zn2+ by oxidants at inflammatory sites may contribute to tissue damage.
  • Dithiothreitol (DTT) demonstrates potential in reversing Zn2+-mediated injury by chelating mobilized zinc.

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