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Identifying the site of the source of reactive oxygen species within the mitochondria after transient exposure of cardiac myocytes to hydrogen peroxide

Viola, H.M., Ingley, E.ORCID: 0000-0002-8112-9134, Arthur, P.G. and Hool, L.C. (2009) Identifying the site of the source of reactive oxygen species within the mitochondria after transient exposure of cardiac myocytes to hydrogen peroxide. Biophysical Journal, 96 (3). 244a.

Link to Published Version: https://doi.org/10.1016/j.bpj.2008.12.1203
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Abstract

Oxidative stress is a feature of cardiovascular disease. Hydrogen peroxide (H2O2) can act as a signaling molecule to mediate cardiovascular pathology. We have previously shown that transient exposure of adult guinea pig ventricular myocytes to H2O2 leads to further production of reactive oxygen species (ROS) from the mitochondria. We have demonstrated that exposure of myocytes to 30μM H2O2 for 5 min then 10U/ml catalase for 5 min to degrade the H2O2 caused a 65.4±8.4% further increase in superoxide by the mitochondria (n=47). We tested whether transient exposure to H2O2 altered protein synthesis in the myocytes. Exposure of myocytes to 30μM H2O2 for 5 min followed by 10U/ml catalase for 5 min caused a 2-fold increase in protein synthesis measured as 3H-Leucine incorporation (n=10). This suggests that a transient exposure to H2O2 may be sufficient to induce cardiac hypertrophy. We now wish to identify the site of ROS production in the mitochondria. Superoxide was assessed with the fluorescent indicator dihydroethidium (DHE). Exposing myocytes to 1μM DPI, which binds prior to the ROS generation site of complex I, followed by transient exposure to H2O2 resulted in complete attenuation of the increase in DHE signal after exposure to H2O2. Exposing myocytes to 1μM rotenone, which binds after the ROS generation site of complex I, followed by transient exposure to H2O2 resulted in a 45% reduction in the increase in DHE signal after exposure to H2O2. These data suggest the source of ROS production is distal to complex I. Identifying the site of production of ROS may represent a possible therapeutic target to prevent the development of cardiac hypertrophy associated with a transient exposure to H2O2.

Item Type: Journal Article
Publisher: Elsevier Inc
Copyright: © 2009 Biophysical Society.
URI: http://researchrepository.murdoch.edu.au/id/eprint/48306
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