Role of oxidative stress in alterations of mitochondrial function in ischemic-reperfused hearts

Makazan, Zhanna; Saini, Harjot K.; Dhalla, Naranjan S.

doi:10.1152/ajpheart.01214.2006

Cited by 63 publications

(61 citation statements)

References 51 publications

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“…The role of oxidative stress in alterations of mitochondria in ischemia-reperfusion injury and in catecholamine-induced changes in cardiac sarcolemmal Ca 2? transport has already been indicated [33,34]. The present study demonstrated that epinephrine administration is associated with oxidative stress as the plasma levels of MDA, a marker of lipid peroxidation, rose significantly upon injecting cumulative doses of epinephrine.…”

Section: Discussionsupporting

confidence: 68%

Antiarrhythmic Effects of Some Antioxidant Vitamins in Rats Injected with Epinephrine

et al. 2009

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Since excessive amounts of catecholamines are known to produce arrhythmias and increase the plasma level of aminochrome, an oxidation product of catecholamines, we tested the hypothesis that antioxidants may reduce the formation of aminochrome and prevent the catecholamine-induced arrhythmias. For this purpose, Sprague-Dawley rats were pretreated orally, with vitamin A or vitamin C for 21 days, and their effects on ventricular arrhythmias induced by a bolus dose or cumulative doses of intravenous epinephrine were examined. Electrocardiogram recording of these animals revealed that pretreatment with either of these vitamins increased the time of onset and decreased the duration of the epinephrine-induced ventricular arrhythmias. Ventricular fibrillations due to high doses of epinephrine were also prevented by the antioxidant pretreatment. Although pretreatment with either vitamin A or vitamin C did not affect the basal malondialdehyde level in control animals, the increase in malondialdehyde level caused by epinephrine administration was significantly reduced by these agents. The elevated level of plasma aminochrome due to epinephrine was also decreased by vitamins A and C treatments. The results indicate that antioxidant may prevent catecholamine-induced arrhythmias by reducing the formation of aminochrome and thus may provide a new strategy for the management of stress-related heart disease.

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Section: Discussionsupporting

confidence: 68%

Antiarrhythmic Effects of Some Antioxidant Vitamins in Rats Injected with Epinephrine

et al. 2009

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“…In addition to the respiratory burst of inflammatory cells such local ischemia can further induce ROS production via xanthine oxidase conversion from xanthine dehydrogenase. (Chanock et al, 1994;Nishino, 1994;Gute et al, 1998;Makazan et al, 2007).Multiple groups have shown that stem cells appear to have an increased antioxidant capacity (Dernbach et al, 2004;He et al, 2004), whereas others have demonstrated the deleterious role of inflammation and oxidative stress in cell transplantation (Qu et al, 1998;Suzuki et al, 2000). Our group has shown that MDSCs have lower rates of stressinduced cell death, and we have speculated that the MDSCs' increased regenerative capacity may relate to an increased resistance to oxidative and inflammatory stress Deasy et al, 2007).…”

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confidence: 78%

Section: Introductionmentioning

confidence: 99%

Antioxidant Levels Represent a Major Determinant in the Regenerative Capacity of Muscle Stem Cells

Urish

Vella

Okada³

et al. 2009

MBoC

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Stem cells are classically defined by their multipotent, long-term proliferation, and self-renewal capabilities. Here, we show that increased antioxidant capacity represents an additional functional characteristic of muscle-derived stem cells (MDSCs). Seeking to understand the superior regenerative capacity of MDSCs compared with myoblasts in cardiac and skeletal muscle transplantation, our group hypothesized that survival of the oxidative and inflammatory stress inherent to transplantation may play an important role. Evidence of increased enzymatic and nonenzymatic antioxidant capacity of MDSCs were observed in terms of higher levels of superoxide dismutase and glutathione, which appears to confer a differentiation and survival advantage. Further when glutathione levels of the MDSCs are lowered to that of myoblasts, the transplantation advantage of MDSCs over myoblasts is lost when transplanted into both skeletal and cardiac muscles. These findings elucidate an important cause for the superior regenerative capacity of MDSCs, and provide functional evidence for the emerging role of antioxidant capacity as a critical property for MDSC survival post-transplantation. INTRODUCTIONMyogenic cell transplantation has been proposed as a promising therapeutic approach in the treatment of skeletal and cardiac muscle injury. Early studies of myoblast transplantation into dystrophic skeletal muscle yielded limited regeneration of dystrophin-expressing muscle fibers (Beauchamp et al., 1994;Gussoni et al., 1997;Qu-Petersen et al., 2002). Similarly, given the limited regenerative ability of cardiac muscle, cell transplantation has been proposed as an alternative to heart transplantation (Assmus et al., 2006;Lunde et al., 2006;Schachinger et al., 2006).A major obstacle in both cardiac and skeletal myogenic therapies is the poor rate of engraftment of myogenic cells after transplantation (Taylor et al., 1998;Oshima et al., 2005). In skeletal muscle, numerous groups have observed a rapid inflammatory response that appears to contribute to rapid cell loss and limit therapeutic success (Beauchamp et al., 1994;Gussoni et al., 1997;Beauchamp et al., 1999). Multiple groups have postulated that the small number of injected cells that survive transplantation in both cardiac and skeletal muscle may represent a special subpopulation of stem-like cells (Qu et al., 1998;Beauchamp et al., 1999;Qu-Petersen et al., 2002).For these reasons, our group attempted to isolate this putative subpopulation of cells using a modified preplate technique. This procedure was initially developed to purify myoblasts from nonmyogenic cells, including fibroblasts, of whole tissue preparations based on the differential adhesion characteristics of the cells to a collagen coated flask (Rando and Blau, 1994). Our group modified this technique to isolate various populations of myogenic cells, including a population of early adhering preplate (EP) cells and a late adhering preplate (LP) cell population from which a subpopulation of long-term proliferating (LTP) cells,...

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“…However, the precise mechanisms underlying the protective effects of CIHH on ischemic hearts are far from clear. It is well known that oxidative stress and oxygen-derived free radicals [primarily reactive oxygen species (ROS)] contribute to I/R injury [10,11] . Many proteins that have key roles in the homeostasis of cardiomyocytes, such as the Na + /Ca 2+ exchanger and the sodium pump, are modified during massive ROS release [12,13] .…”

Section: Introductionmentioning

confidence: 99%

Chronic intermittent hypobaric hypoxia protects the heart against ischemia/reperfusion injury through upregulation of antioxidant enzymes in adult guinea pigs

Guo

Zhang

et al. 2009

Acta Pharmacol Sin

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Aim: To investigate the protection and the anti-oxidative mechanism afforded by chronic intermittent hypobaric hypoxia (CIHH) against ischemia/reperfusion (I/R) injury in guinea pig hearts. Methods: Adult male guinea pigs were exposed to CIHH by mimicking a 5000 m high altitude (p B =404 mmHg, p O2 =84 mmHg) in a hypobaric chamber for 6 h/day for 28 days. Langendorff-perfused isolated guinea pig hearts were used to measure variables of left ventricular function during baseline perfusion, ischemia and the reperfusion period. The activity and protein expression of antioxidant enzymes in the left myocardium were evaluated using biochemical methods and Western blotting, respectively. Intracellular reactive oxygen species (ROS) were assessed using ROS-sensitive fluorescence. Results: After 30 min of global no-flow ischemia followed by 60 min of reperfusion, myocardial function had better recovery rates in CIHH guinea pig hearts than in control hearts. The activity and protein expression of superoxide dismutase (SOD) and catalase (CAT) were significantly increased in the myocardium of CIHH guinea pigs. Pretreatment of control hearts with an antioxidant mixture containing SOD and CAT exerted cardioprotective effects similar to CIHH. The irreversible CAT inhibitor aminotriazole (ATZ) abolished the cardioprotection of CIHH. Cardiac contractile dysfunction and oxidative stress induced by exogenous hydrogen peroxide (H 2 O 2 ) were attenuated by CIHH and CAT. Conclusions: These data suggest that CIHH protects the heart against I/R injury through upregulation of antioxidant enzymes in guinea pig.

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Role of oxidative stress in alterations of mitochondrial function in ischemic-reperfused hearts

Cited by 63 publications

References 51 publications

Antiarrhythmic Effects of Some Antioxidant Vitamins in Rats Injected with Epinephrine

Antiarrhythmic Effects of Some Antioxidant Vitamins in Rats Injected with Epinephrine

Antioxidant Levels Represent a Major Determinant in the Regenerative Capacity of Muscle Stem Cells

Chronic intermittent hypobaric hypoxia protects the heart against ischemia/reperfusion injury through upregulation of antioxidant enzymes in adult guinea pigs

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