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Cardiovascular Research 1999 42(3):576-577; doi:10.1016/S0008-6363(99)00048-6
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Cytokine-induced free radicals and their roles in myocardial dysfunctions

Ghassan Bkailya,* and Pedro D’orléans-Justeb

aMRCC Group in Immuno–Cardiovascular Interaction, Department of Anatomy and Cell Biology, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Québec, Canada J1H 5N4
bDepartment of Pharmacology, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Québec, Canada, J1H 5N4

gbkail01@courrier.usherb.ca

* Corresponding author

Received 22 January 1999; accepted 2 February 1999

The first 10% of the full text of this article appears below.

See article of Cheng et al. [9] (pages 651–659) in this issue.

Recent studies dealing with oxygen free radicals and nitric oxide (NO) have demonstrated their implications in diseases such as inflammation, ischemia–reperfusion injury and several other cardiovascular dysfunctions [1–4].

Activated oxygen species, such as singlet oxygen, superoxide anion (O2–), hydrogen peroxide (H2O2) and hydroxyl radical (OH–) are highly unstable, extremely reactive and highly toxic [4]. Superoxide anions are usually required for the generation of H2O2 and OH–. The generation of free radicals is a normal physiological phenomenon, which is controlled by naturally occurring scavengers produced by the cell such as superoxide dismutase (SOD), glutathione peroxidase (GSHPx), catalase . . . [Full Text of this Article]


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