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Maulik N, Watanabe M, Engelman DT, et al. Oxidative stress adaptation improves postischemic ventricular recovery. Mol Cell Biochem. 1995;144(1):67-74doi: 10.1007/BF00926742.
Maulik, N., Watanabe, M., Engelman, D. T., Engelman, R. M., & Das, D. K. (1995). Oxidative stress adaptation improves postischemic ventricular recovery. Molecular and cellular biochemistry, 144(1), 67-74. https://doi.org/10.1007/BF00926742
Maulik, N, et al. "Oxidative stress adaptation improves postischemic ventricular recovery." Molecular and cellular biochemistry vol. 144,1 (1995): 67-74. doi: https://doi.org/10.1007/BF00926742
Maulik N, Watanabe M, Engelman DT, Engelman RM, Das DK. Oxidative stress adaptation improves postischemic ventricular recovery. Mol Cell Biochem. 1995 Mar 09;144(1):67-74. doi: 10.1007/BF00926742. PMID: 7791747.
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Mol Cell Biochem. 1995 Mar 09;144(1):67-74. doi: 10.1007/BF00926742.

Oxidative stress adaptation improves postischemic ventricular recovery.

Molecular and cellular biochemistry

N Maulik, M Watanabe, D T Engelman, R M Engelman, D K Das

Affiliations

  1. Department of Surgery, University of Connecticut School of Medicine, Farmington 06030, USA.

PMID: 7791747 DOI: 10.1007/BF00926742

Abstract

Adaptation to various forms of stress has been found to be associated with increased cellular tolerance to myocardial ischemia. In this study, the effects of myocardial adaptation to oxidative stress was examined by injecting rats with endotoxin (0.5 mg/kg) and its non-toxic derivative, lipid A (0.5 mg/kg). Both compounds exerted oxidative stress within 1 h of treatment as evidenced by enhanced malonaldehyde formation. The oxidative stress disappeared steadily and progressively with time in concert with the appearance of the induction of glutathione and antioxidative enzymes that included superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase. After 24 h of endotoxin or lipid A treatment, the amount of oxidative stress and antioxidant enzyme levels were significantly lower and higher, respectively, compared to those at the baseline levels. Corroborating these results, both endotoxin and lipid A provided protection against myocardial ischemia and reperfusion injury as evidenced by a significantly improved postischemic recovery of left ventricular functions. The data presented here demonstrates that a controlled amount of oxidative stress induces the expression of intracellular antioxidants that can result in enhanced myocardial tolerance to ischemia. This suggests that myocardial adaptation to oxidative stress may be a potential tool for reduction of ischemic/reperfusion injury.

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