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1 Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, Connecticut, United States
2 Inst. of Environmental Medicine, Univ. Pennsylvania, Philadelphia, Pennsylvania, United States
* To whom correspondence should be addressed. E-mail: ddas{at}neuron.uchc.edu.
Peroxiredoxin 6 [PRDX6] is a novel peroxidase enzyme belonging to PRDX family, which contains five more peroxiredoxins [PRDX1-PRDX5]. Like glutathione peroxidase and catalase, PRDX6 possesses H2O2 scavenging activities; and like the former, it also removes hydroperoxides. Since significant amounts of catalase and GSHPx are present in the hearts contributing towards the attenuation of H2O2 and hydroperoxides formed during ischemia-reperfusion injury and thereby providing cardioprotection, we asked whether PRDX6 also has any role in this process. In the present study we used PRDX6-/- mouse to assess the role of PRDX6 in ischemic injury. Western blot analysis revealed complete absence of any PRDX activity in the PRDX6-/- mouse heart while the GSHPx-1 and catalase levels remained unchanged. Randomly selected hearts from PRDX6-/- mice and wild type mice were subjected to 30 min of global ischemia followed by 120 min of reperfusion at normothermia. The hearts from the PRDX6-/- mice appeared to be more susceptible to the ischemic reperfusion injury as evidenced by reduced recovery of left ventricular function, greater myocardial infarct size and higher amount of apoptotic cardiomyocytes as compared to wild type mouse hearts. These PRDX6-/- hearts were also subjected to higher amount of oxidative stress as evidenced by the present of higher amount of MDA in these hearts. The present study, thus, indicates a non-redundant role of PRDX6 in myocardial ischemic reperfusion injury as catalase and GSHPx could not make up for the deficiency of PRDX6 activities.
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