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• W2015951477 abstract "Increased oxidative stress may contribute to the pathogenesis of cardiovascular disease, and clinical and experimental studies have suggested that these diseases are associated with oxidative damage in either cardiac and aortic cells due to increased formation of free radicals and/or reduction of the antioxidant defenses [[1]de Lorgeril M. Salen P. Accominotti M. et al.Dietary and blood antioxidants in patients with chronic heart failure. Insights into the potential importance of selenium in heart failure.Eur J Heart Fail. 2001; 3: 661-669Crossref PubMed Scopus (97) Google Scholar]. Oxidative stress in obese individuals increases the susceptibility to oxidative damage. Several studies have shown a high level of ROS in obese individuals [2Van Gaal L.F. Vertommen J. De Leeuw I.H. The in vitro oxidizability of lipoprotein particles in obese and non-obese subjects.Atherosclerosis. 1998; 137: S39-S44Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar, 3Skrha J. Sindelka G. Kvasnicka J. Hilgertova J. Insulin action and fibrinolysis influenced by vitamin E in obese Type 2 diabetes mellitus.Diabetes Res Clin Pract. 1999; 44: 27-33Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar, 4Ozata M. Mergen M. Oktenli C. et al.Increased oxidative stress and hypozincemia in male obesity.Clin Biochem. 2002; 35: 627-631Crossref PubMed Scopus (222) Google Scholar]. Although the role of antioxidant system remains uncertain concerning prevention or protection against the tissue damage induced by myocardial infarction, accumulating evidence demonstrates that the deficiency on antioxidant system renders the heart vulnerable to ischemia–reperfusion injury in animal models [5Nagy N. Malik G. Fisher A.B. Das D.K. Targeted disruption of peroxiredoxin 6 gene renders the heart vulnerable to ischemia-reperfusion injury.Am J Physiol Heart Circ Physiol. 2006; 291: H2636-H2640Crossref PubMed Scopus (68) Google Scholar, 6Yoshida T. Maulik N. Engelman R.M. Ho Y.S. Das D.K. Targeted disruption of the mouse Sod I gene makes the hearts vulnerable to ischemic reperfusion injury.Circ Res. 2000; 86: 264-269Crossref PubMed Scopus (104) Google Scholar]. Exercise training induces cardioprotection against myocardial ischemia–reperfusion injury [[7]Powers S.K. Quindry J. Hamilton K. Aging, exercise, and cardioprotection.Ann N Y Acad Sci. 2004; 1019: 462-470Crossref PubMed Scopus (57) Google Scholar]; however, the role of antioxidant response induced by exercise is unknown. Recently, we demonstrated that chronic exercise reduces ROS and increased the survival in lean rats submitted to experimental infarction [[8]Frederico M.J. Justo S.L. Da Luz G. et al.Exercise training provides cardioprotection via a reduction in reactive oxygen species in rats submitted to myocardial infarction induced by isoproterenol.Free Radic Res. 2009; 43: 957-964Crossref PubMed Scopus (22) Google Scholar]. However, the cardioprotective effects of exercise training (ET) and oxidative stress in obese rats have not been investigated. Thus, we sought to determine the effects of ET on oxidative stress in myocardial and aorta of obese rats submitted to experimental infarction. Male Wistar rats were fed on standard chow or high fat-diet for two months, as previously described [[9]De Souza C.T. Araujo E.P. Prada P.O. Saad M.J. Boschero A.C. Velloso L.A. Short-term inhibition of peroxisome proliferator-activated receptor-gamma coactivator-1alpha expression reverses diet-induced diabetes mellitus and hepatic steatosis in mice.Diabetologia. 2005; 48: 1860-1871Crossref PubMed Scopus (29) Google Scholar]; thereafter, obese rats were submitted to exercise training (nine-channel motor-drive treadmill at 1 km/h for 50 min/d, 5 d/wk) for two months (Fig. 1A ). As expected, high-fat diet increased the total body weight and epidydimal fat weight in rats (Fig. 1B and C). Exercise training did not change total body weight, though it reduced epidydimal fat content (Fig. 1B and C). At the end of the exercise protocol, high levels of superoxide anion, TBARS and carbonyl were found in myocardial and aorta of obese animals, compared with the lean group. Conversely, exercise reduced these oxidative stress markers in myocardial tissue and aorta in obese animals, when compared with the obese group at rest (Fig. 1D-I). This data are in accordance with previous studies performed in lean animals [8Frederico M.J. Justo S.L. Da Luz G. et al.Exercise training provides cardioprotection via a reduction in reactive oxygen species in rats submitted to myocardial infarction induced by isoproterenol.Free Radic Res. 2009; 43: 957-964Crossref PubMed Scopus (22) Google Scholar, 10French J.P. Hamilton K.L. Quindry J.C. Lee Y. Upchurch P.A. Powers S.K. Exercise-induced protection against myocardial apoptosis and necrosis: MnSOD, calcium-handling proteins, and calpain.FASEB J. 2008; 22: 2862-2871Crossref PubMed Scopus (101) Google Scholar]. Next, we investigated antioxidant enzyme activity, such as, SOD, GPx and catalase. These assays were performed as previously described [[8]Frederico M.J. Justo S.L. Da Luz G. et al.Exercise training provides cardioprotection via a reduction in reactive oxygen species in rats submitted to myocardial infarction induced by isoproterenol.Free Radic Res. 2009; 43: 957-964Crossref PubMed Scopus (22) Google Scholar]. SOD and GPx activities were reduced in myocardial and aorta tissues of the obese group, when compared with the lean animals. However, the chronic exercise increased the activity of these enzymes in both tissues of obese animals, when compared with the obese group at rest (Fig. 1J–M). These data are important, for a number of reasons. First, a reduction in CuZn-SOD and GPx activity and protein levels was observed in human erythrocyte from obese subjects, compared to normal weight individuals [4Ozata M. Mergen M. Oktenli C. et al.Increased oxidative stress and hypozincemia in male obesity.Clin Biochem. 2002; 35: 627-631Crossref PubMed Scopus (222) Google Scholar, 11Olusi S.O. Obesity is an independent risk factor for plasma lipid peroxidation and depletion of erythrocyte cytoprotectic enzymes in humans.Int J Obes Relat Metab Disord. 2002; 26: 1159-1164Crossref PubMed Scopus (278) Google Scholar]. Second, high level of superoxide anion was observed in the endothelium of the coronary arteries of obese animals, and it was related to endothelial dysfunction [[12]Galili O. Versari D. Sattler K.J. et al.Early experimental obesity is associated with coronary endothelial dysfunction and oxidative stress.Am J Physiol Heart Circ Physiol. 2007; 292: H904-H911Crossref PubMed Scopus (152) Google Scholar]. Third, a high production of superoxide ventricular is coupled with a decrease in cardiac function [[13]Khadour F.H. Panas D. Ferdinandy P. et al.Enhanced NO and superoxide generation in dysfunctional hearts from endotoxemic rats.Am J Physiol Heart Circ Physiol. 2002; 283: H1108-H1115PubMed Google Scholar]. Finally, Sod−/− mouse hearts were more susceptible to ischemic reperfusion injury [[6]Yoshida T. Maulik N. Engelman R.M. Ho Y.S. Das D.K. Targeted disruption of the mouse Sod I gene makes the hearts vulnerable to ischemic reperfusion injury.Circ Res. 2000; 86: 264-269Crossref PubMed Scopus (104) Google Scholar]. Thus, the cardioprotective mechanism of exercise in obese on endothelial and myocardial dysfunction could be associated with reduced oxidative stress and increased capacity of antioxidant enzymes [[14]De Nigris F. Demontis M.P. Rodriguez-Porcel M. Anania V. Lerman L.O. Napoli C. Renal blood flow in hypercholesterolemic pigs is increased by chronic antioxidant treatment.J Vet Pharmacol Ther. 2003; 26: 113-116Crossref PubMed Scopus (4) Google Scholar]. On the other hand, catalase activity was similar in myocardial tissues of both groups (Fig. 1N). We observed that catalase activity was increased in aorta of obese exercised animals, when compared with the obese group at rest (Fig. 1O). Our results regarding SOD and catalase activity in myocardial of exercised animals are in accordance with the study published by Hong and Johnson [[15]Hong H. Johnson P. Antioxidant enzyme activities and lipid peroxidation levels in exercised and hypertensive rat tissues.Int J Biochem Cell Biol. 1995; 27: 923-931Crossref PubMed Scopus (46) Google Scholar]. The authors also observed an increase in cardiac activity of SOD in exercised animals, but activity of CAT remained unchanged [[15]Hong H. Johnson P. Antioxidant enzyme activities and lipid peroxidation levels in exercised and hypertensive rat tissues.Int J Biochem Cell Biol. 1995; 27: 923-931Crossref PubMed Scopus (46) Google Scholar]. It is important to note that, although studies indicate that antioxidants improve heart muscle function, its adaptation to the antioxidant system depends on tissue analyzed and type, intensity and duration of exercise [[16]Powers S.K. Criswell D. Lawler J. et al.Rigorous exercise training increases superoxide dismutase activity in ventricular myocardium.Am J Physiol. 1993; 265: H2094-H2098PubMed Google Scholar]. Western blotting analysis showed that SOD and Catalase protein levels were similar among the groups in both tissues (Fig. 1P). In myocardial tissue, GPx protein expression was reduced by about 70% in obese animals, when compared to the lean group; however, exercise restored the GPx expression in myocardial tissue of obese animals (Fig. 1P). GPx expression was similar in aortas of both groups (Fig. 1P). These findings showed that the effects of exercise on the myocardium and aorta of obese rats appear to occur at the level of enzyme activity rather than the protein levels. Since the deficiency of antioxidant response is associated with vulnerability of the myocardial infarction and ischemia–reperfusion injury [6Yoshida T. Maulik N. Engelman R.M. Ho Y.S. Das D.K. Targeted disruption of the mouse Sod I gene makes the hearts vulnerable to ischemic reperfusion injury.Circ Res. 2000; 86: 264-269Crossref PubMed Scopus (104) Google Scholar, 8Frederico M.J. Justo S.L. Da Luz G. et al.Exercise training provides cardioprotection via a reduction in reactive oxygen species in rats submitted to myocardial infarction induced by isoproterenol.Free Radic Res. 2009; 43: 957-964Crossref PubMed Scopus (22) Google Scholar], we sought to determine whether antioxidant effects of exercise could increase the survival during experimental infarction in obese animals. Thus, 48 h after the last session of exercise, lean, obese and exercised obese rats were submitted to infarction by using subcutaneous injection of isoproterenol hydrochloride (60 mg/kg) (n=10 animals per group). We observed that obese group presented high levels of mortality (p<0.001), when compared with lean rats. Only one obese animal survived after experimental infarction. Interestingly, exercise increased the rate of survival of infarcted animals, when compared to the obese group at rest (Fig. 1Q). The increase in survival rate in exercised animals after the experimental infarction occurred, at least in part, due to the modulation of the antioxidant system, though we cannot exclude the possibility that other factors, such as anti-inflammatory action, structural and functional myocardial and vascular adaptation could be associated with this phenomenon. Collectively, exercise training resulted in low formation of superoxide anion and minor damage to lipids and proteins, probably due to increased activity of SOD and GPx. Furthermore, the reduction in percentage of death in obese rats may be related to lower levels of oxidative stress, as a cardioprotective mechanism." @default.
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• W2015951477 title "Exercise training plays cardioprotection through the oxidative stress reduction in obese rats submitted to myocardial infarction" @default.
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