Hydrogen sulphide: a novel physiological inhibitor of LDL atherogenic modification by HOCl |
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| Authors: | Laggner Hilde Muellner Markus K Schreier Sabine Sturm Brigitte Hermann Marcela Exner Markus Gmeiner Bernhard M K Kapiotis Stylianos |
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| Institution: |
a Department of Medical Chemistry, Centre of Physiology and Pathophysiology, Medical University Vienna, Vienna, Austria
b Department of Medical Biochemistry, Max F. Perutz Laboratories, Medical University Vienna, Vienna, Austria
c Clinical Institute of Medical and Chemical Laboratory Diagnostics, AKH “Die Menschliche Groesse”, Medical University Vienna, Vienna, Austria
d The Central Laboratory, Hospital of the Divine Redeemer, Vienna, Austria |
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| Abstract: | Hypochlorite (HOCl), the product of the activated myeloperoxidase/H2O2/chloride (MPO/H2O2/Cl- ) system is favored as a trigger of LDL modifications, which may play a pivotal role in early atherogenesis. As HOCl has been shown to react with thiol-containing compounds like glutathione and N-acetylcysteine protecting LDL from HOCl modification, we have tested the ability of hydrogen sulfide (H2S)—which has recently been identified as an endogenous vasorelaxant—to counteract the action of HOCl on LDL. The results show that H2S could inhibit the atherogenic modification of LDL induced by HOCl, as measured by apolipoprotein alterations. Beside its HOCl scavenging potential, H2S was found to inhibit MPO (one may speculate that this occurs via H2S/heme interaction) and destroy H2O2. Thus, H2S may interfere with the reactants and reaction products of the activated MPO/H2O2/Cl- system. Our data add to the evidence of an anti-atherosclerotic action of this gasotransmitter taking the role of HOCl in the atherogenic modification of LDL into account. |
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| Keywords: | LDL hypochlorite hydrogen sulphide atherosclerosis |
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