Antioxidants

Targeting Endogenous Antioxidants to Prevent Cardiovascular Diseases

1. W. H. Wilson Tang

+Author Affiliations

1. Center for Cardiovascular Diagnostics and Prevention, Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic Cleveland, OH
2. Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH

1. Correspondence to:
   W. H. Wilson Tang, MD, 9500 Euclid Avenue, Desk J3-4, Cleveland, OH 44195. E-mail: tangw@ccf.org

• Oxidative stress has long been associated with a wide range of cardiovascular risk factors and likely contributes to the progression of cardiovascular diseases in animal models and in humans.¹ Numerous lines of evidence indicate that pathways of oxidative and nitrative stress can contribute to cardiovascular disease via multiple mechanisms, such as through formation of atherogenic lipoproteins, initiation of lipid oxidation, and propagation of damage to endothelial cells and myocytes.¹ Nevertheless, quantifying the degree of oxidative stress has posed major challenges because many of these processes occur intracellularly and involve complicated issues with stability and variability in biospecimens. Hence, the identification of biomarkers of oxidative stress has focused on detecting systemic stable oxidized products (eg, oxidized low-density lipoprotein, F2-isoprostanes) or identifying the presence of mediators of oxidative stress pathways (eg, oxidation of nitric oxide by myeloperoxidase² and ceruloplasmin³). In addition, quantifying the activities of endogenous antioxidant proteins such as high-density lipoprotein–associated paraoxonase-1 activities⁴ or glutathione⁵may reflect underlying oxidative imbalance. Indeed, large prospective cohorts have identified individuals with abnormal levels of several of the aforementioned biomarkers to be at greater risk for future cardiovascular risks.^2–5/.../