[Protection of oxidation of LDL by nitric oxide: implication in atherogenesis].
Superoxide (O2-) and nitric oxide (.NO) are free radicals which are known to react together leading to peroxynitrite anions that can decompose to form nitrogen dioxide (NO2) and hydroxyl radical (OH degrees). .NO has been reported to have a dual effect on LDL oxidation (pro or antioxidant). In the present study we have investigated in vitro the action of exogenous .NO on human LDL oxidation promoted by oxygen, copper or (2,2'-azobis (2-aminodinopropane hydrochloride)(ABAP). .NO was given as NO donnor (sodium nitroprussiate or S-nitroso-L-glutathione) from 10 to 500 microM. Oxidation of LDL was measured by monitoring continuously conjugated diene formation at 234 nm. Exogenous .NO inhibited in a dose dependent manner the progress of spontaneous LDL oxidation. Copper--or ABAP--induced oxidation were characterized by lag, propagation and decomposition phases. Exogenous .NO decreased the propagation rate of LDL oxidation and the level of maximal diene production. These effects are different of these of alpha-tocopherol, a chain-breaking antioxidant. In our experimental conditions, .NO exhibited antioxidant activities. In vivo, the continuous release of endogenous .NO could protect LDL from cell-induced oxidation.
INSERM U58, Hôpital Lapeyronie, Montpellier.
M F
MF
Maggi
J P
JP
Cristol
M C
MC
Guérin
B
B
Descomps
J
J
Torreilles
D000577:Amides / Q000494:pharmacology; D000578:Amidines / Q000494:pharmacology; D001161:Arteriosclerosis / Q000503:physiopathology*; D003300:Copper / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D006801:Humans; D066298:In Vitro Techniques; D008077:Lipoproteins, LDL / Q000502:physiology*; D009569:Nitric Oxide / Q000008:administration & dosage / Q000494:pharmacology*; D010084:Oxidation-Reduction; D014810:Vitamin E / Q000032:analysis
D000577:Amides; D000578:Amidines; D008077:Lipoproteins, LDL; D014810:Vitamin E; D009569:Nitric Oxide; C046728:2,2'-azobis(2-amidinopropane); D003300:Copper
Protection de l'oxydation des LDL par le monoxyde d'azote implications dans l'athérogenèse.