title: Reactive oxygen species and the cardiovascular system.
abstract: Ever since the discovery of free radicals, many hypotheses on the deleterious actions of reactive oxygen species (ROS) have been proposed. However, increasing evidence advocates the necessity of ROS for cellular homeostasis. ROS are generated as inherent by-products of aerobic metabolism and are tightly controlled by antioxidants. Conversely, when produced in excess or when antioxidants are depleted, ROS can inflict damage to lipids, proteins, and DNA. Such a state of oxidative stress is associated with many pathological conditions and closely correlated to oxygen consumption. Although the deleterious effects of ROS can potentially be reduced by restoring the imbalance between production and clearance of ROS through administration of antioxidants (AOs), the dosage and type of AOs should be tailored to the location and nature of oxidative stress. This paper describes several pathways of ROS signaling in cellular homeostasis. Further, we review the function of ROS in cardiovascular pathology and the effects of AOs on cardiovascular outcomes with emphasis on the so-called oxidative paradox.
authors.affiliation: Department of Experimental Cardiology, Erasmus Medical Center Rotterdam, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands. taverneyannick@yahoo.co.uk
authors.forename: Yannick J H J
authors.initials: YJ
authors.lastname: Taverne
authors.forename: Ad J J C
authors.initials: AJ
authors.lastname: Bogers
authors.forename: Dirk J
authors.initials: DJ
authors.lastname: Duncker
authors.forename: Daphne
authors.initials: D
authors.lastname: Merkus
mesh_terms: D000818:Animals; D002319:Cardiovascular System / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002477:Cells / Q000378:metabolism; D006801:Humans; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D017382:Reactive Oxygen Species