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Role of Oxidative Stress in Subcellular Defects in Ischemic Heart Disease

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Biochemistry of Oxidative Stress

Part of the book series: Advances in Biochemistry in Health and Disease ((ABHD,volume 16))

Abstract

Ischemic heart disease is caused by obstruction of the coronary arteries that reduces myocardial perfusion. The most efficient way to restore blood supply to the ischemic myocardium is reperfusion of the affected area. However, if reperfusion is initiated too late, it enhances ischemia-reperfusion damage to the heart. Oxidative stress is one of the major causes for the development of ischemia-reperfusion (I/R) injury to the heart, which is characterized by decreased functional performance, ultrastructural changes and metabolic alterations. Excessive formation of oxyradicals during the development of I/R injury has now been shown to produce a wide variety of abnormalities in cardiac subcellular organelles such as sarcolemma, sarcoplasmic reticulum, mitochondria and myofibrils. Different reactive oxygen species (ROS) have been shown to cause alterations in several proteins leading to their malfunction and changes in enzyme activities. Lipid peroxidation leads to depressed membrane fluidity and increased permeability, as well as changes in gene expression leading to impaired recovery of cardiac dysfunction due to I/R injury. Since the redox status of cardiomyocytes depends mainly on the balance between ROS production and availability of endogenous antioxidant defense systems, extensive efforts are made to maintain the redox status during I/R injury. Cardioprotection by ischemic conditioning as well as treatment of the heart with exogenous antioxidants have been observed to result in the increased availability of endogenous antioxidants and prevent oxidative damage to subcellular organelles. Thus antioxidant therapy is considered to be a promising strategy to decrease the I/R induced damage to the heart. Accordingly, this article is intended to describe the mechanisms of oxidative stress induced subcellular defects leading to cardiac dysfunction due to I/R injury and to outline the role of antioxidant defense mechanisms in the prevention as well as treatment of the ischemic heart disease.

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Authors and Affiliations

  1. Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovak Republic

    Monika Bartekova & Miroslav Barancik

  2. Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre, Department of Physiology and Pathophysiology, Max Rady College of Medicine, University of Manitoba, Winnipeg, Canada

    Naranjan S. Dhalla

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  1. Monika Bartekova
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  2. Miroslav Barancik
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  3. Naranjan S. Dhalla
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Correspondence to Naranjan S. Dhalla .

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Editors and Affiliations

  1. School of Medicine, University of Buenos Aires, Buenos Aires, Argentina

    Ricardo Jorge Gelpi

  2. School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Argentina

    Alberto Boveris

  3. Instituto de Inmunología, Genética y Metabolismo (INIGEM, UBA–CONICET), Laboratorio de Metabolismo del Oxígeno, Hospital Universitario, Universidad de Buenos Aires, Buenos Aires, Argentina

    Juan José Poderoso

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Bartekova, M., Barancik, M., Dhalla, N.S. (2016). Role of Oxidative Stress in Subcellular Defects in Ischemic Heart Disease. In: Gelpi, R., Boveris, A., Poderoso, J. (eds) Biochemistry of Oxidative Stress. Advances in Biochemistry in Health and Disease, vol 16. Springer, Cham. https://doi.org/10.1007/978-3-319-45865-6_9

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