title: S-nitrosothiols do not induce oxidative stress, contrary to other nitric oxide donors, in cultures of vascular endothelial or smooth muscle cells.
abstract: Nitric oxide (NO) has been described to exert various anti-atherogenic actions. However, NO, in some cases, has been shown to stimulate the oxidation of low-density lipoprotein (LDL), which constitute an important triggering event in atherosclerosis. Thus, some NO donors, despite their advantages, might also induce oxidative stress. Therefore, the purpose of this study is to examine the effect of three different NO donors on LDL oxidation, in acellular system as well as in cultures of normal endothelial cells or smooth muscle cells, which constitute the two major cellular components of the arterial wall. Sodium nitroprusside oxidized strongly LDL in medium alone as well as in endothelial or smooth muscle cell cultures. Sydnonimine-1 (SIN-1) oxidized LDL already in the absence of cells and enhanced clearly the LDL oxidation in the cultures. S-nitroso-N-acetylpenicillamine was unable to oxidize LDL in synthetic medium alone as well as in the presence of cells, showing that the amount of superoxide and other reactive oxygen species released by these cells did not suffice, contrary to those liberated by macrophages, to combine to NO providing oxidant activity.
authors.affiliation: Laboratoire de Biologie cellulaire (BANI/CELL), Université Catholique de Louvain (UCL), Place Croix du Sud, 5, B 1348 Louvain-La Neuve, Belgium.
authors.forename: K
authors.initials: K
authors.lastname: Jaworski
authors.forename: F
authors.initials: F
authors.lastname: Kinard
authors.forename: D
authors.initials: D
authors.lastname: Goldstein
authors.forename: P
authors.initials: P
authors.lastname: Holvoet
authors.forename: A
authors.initials: A
authors.lastname: Trouet
authors.forename: Y J
authors.initials: YJ
authors.lastname: Schneider
authors.forename: C
authors.initials: C
authors.lastname: Remacle
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D003676:Deferoxamine / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D016166:Free Radical Scavengers / Q000494:pharmacology; D007502:Iron Chelating Agents / Q000494:pharmacology; D008077:Lipoproteins, LDL / Q000378:metabolism; D008981:Molsidomine / Q000031:analogs & derivatives* / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D020030:Nitric Oxide Donors / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D026423:S-Nitroso-N-Acetylpenicillamine / Q000494:pharmacology; D026403:S-Nitrosothiols / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000494:pharmacology; D013552:Swine; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D016166:Free Radical Scavengers; D007502:Iron Chelating Agents; D008077:Lipoproteins, LDL; D020030:Nitric Oxide Donors; D026403:S-Nitrosothiols; D017392:Thiobarbituric Acid Reactive Substances; C099252:oxidized low density lipoprotein; D009599:Nitroprusside; D009569:Nitric Oxide; C002385:linsidomine; D026423:S-Nitroso-N-Acetylpenicillamine; D008981:Molsidomine; D013482:Superoxide Dismutase; D003676:Deferoxamine