title: The protective effect of 17 beta-estradiol on vasomotor responses of aorta from cholesterol-fed rabbit is reduced by inhibitors of superoxide dismutase and catalase.
abstract: The involvement of endogenous antioxidant enzymes in the protective effect of 17 beta-estradiol against hypercholesterolemia was evaluated on aorta from cholesterol-fed rabbits treated with estradiol. 17 beta-Estradiol, more potent than alpha-tocopherol, restored the acetylcholine-induced relaxation, which was impaired by cholesterol chow, and enhanced the vasorelaxation induced by sodium nitroprusside. Diethyldithiocarbamate (5 mM), a superoxide dismutase (SOD) inhibitor, reduced relaxation to acetylcholine down to the level obtained in cholesterol-fed rabbits not treated with estrogen. This inhibition was dose-dependently reversed by addition of exogenous SOD. Aminotriazole (5 mM), a catalase inhibitor, reduced slightly this response, which was not reversed by exogenous catalase. A similar concentration of diethyldithiocarbamate prevented the potentiation of response to sodium nitroprusside induced by estrogen, whereas aminotriazole had no effect. These results suggest that, on aorta from cholesterol-fed rabbit, superoxide dismutase and catalase are involved in the protective effect of estrogen on the vasomotor response to acetylcholine, but only superoxide dismutase participates in response to sodium nitroprusside.
authors.affiliation: Laboratoire de Pharmacologie, Faculté de Pharmacie, Limoges, France.
authors.forename: K
authors.initials: K
authors.lastname: Ghanam
authors.forename: J
authors.initials: J
authors.lastname: Javellaud
authors.forename: L
authors.initials: L
authors.lastname: Ea-Kim
authors.forename: N
authors.initials: N
authors.lastname: Oudart
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000640:Amitrole / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000187:drug effects* / Q000502:physiology*; D002374:Catalase / Q000037:antagonists & inhibitors*; D002784:Cholesterol / Q000097:blood; D002791:Cholesterol, Dietary / Q000008:administration & dosage*; D004036:Diet, Atherogenic; D004050:Ditiocarb / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004958:Estradiol / Q000494:pharmacology*; D006146:Guanidines / Q000494:pharmacology; D006937:Hypercholesterolemia / Q000097:blood / Q000503:physiopathology / Q000517:prevention & control; D066298:In Vitro Techniques; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D009599:Nitroprusside / Q000494:pharmacology; D011817:Rabbits; D013482:Superoxide Dismutase / Q000037:antagonists & inhibitors*; D014280:Triglycerides / Q000097:blood; D014664:Vasodilation / Q000187:drug effects* / Q000502:physiology
chemical_list: D002791:Cholesterol, Dietary; D004791:Enzyme Inhibitors; D006146:Guanidines; D014280:Triglycerides; D009599:Nitroprusside; D004958:Estradiol; D002784:Cholesterol; D004050:Ditiocarb; D002374:Catalase; D019001:Nitric Oxide Synthase; D013482:Superoxide Dismutase; D000109:Acetylcholine; C004479:pimagedine; D019331:NG-Nitroarginine Methyl Ester; D000640:Amitrole