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(Circulation. 2001;103:782.)
© 2001 American Heart Association, Inc.

Editorial

Antioxidants and Myocardial Contractility

Illuminating the "Dark Side" of -Adrenergic Receptor Activation?

Michael M. Givertz, MD; Douglas B. Sawyer, MD, PhD; Wilson S. Colucci, MD

From the Cardiomyopathy Program and Cardiovascular Section, Boston University Medical Center, and Boston University School of Medicine, Boston, Mass.

Correspondence to Wilson S. Colucci, MD, Cardiovascular Section, Boston University Medical Center, 88 E. Newton Street, Boston, MA 02118. E-mail wilson.colucci@bmc.org

Key Words: Editorials • antioxidants • contractility • receptors, adrenergic, beta • myocardium

Oxidant byproducts, such as superoxide anion (O₂^–) and hydrogen peroxide, are produced as a consequence of normal aerobic metabolism. These molecules, which are highly reactive with other biological molecules, are referred to as reactive oxygen species (ROS). Under normal physiological conditions, ROS production is balanced by an efficient system of antioxidants, molecules that are capable of scavenging ROS and thereby preventing oxidant damage. At the cellular level, naturally occurring enzymatic antioxidants such as superoxide dismutase, glutathione peroxidase, and catalase play an important role in the conversion of ROS to oxygen and water. Several nonenzymatic antioxidants, including the lipid-soluble antioxidants vitamin E and -carotene and the water-soluble antioxidants vitamin C and glutathione, are also important in scavenging free radicals. Vitamin C in particular protects plasma lipids from peroxidation, scavenges O₂^–, and plays a role in recycling vitamin E.

In pathological states, ROS may be present in relative excess. This shift of the balance in favor of oxidation, termed "oxidative stress," may have detrimental effects on cellular and tissue function. Oxidative stress is thought to contribute to the pathogenesis of a wide variety of disease states, including atherosclerosis¹ and cancer, as well as to the normal process of aging. There is increasing evidence that myocardial oxidative stress may contribute to disease progression in heart failure.² Although the effects of oxidative stress on the myocardium have been investigated in pathological states, very little is known about the role of ROS in the regulation of normal cardiac function. Recently, Ekelund et al³ . . . [Full Text of this Article]

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