title: Extracellular superoxide dismutase deficiency and atherosclerosis in mice.
abstract: Lipoprotein peroxidation in the arterial wall has been implicated in atherogenesis. The superoxide radical is formed in arteries and can induce such oxidation. Extracellular superoxide dismutase (EC-SOD) occurs in high concentration in the vascular wall interstitium, and in this study, we examined the importance of the enzyme in atherogenesis. On an apolipoprotein E-null background, the limited aortic lesions induced by a 1-month atherogenic diet were larger in EC-SOD wild-type mice than in EC-SOD-null mice, whereas there were no differences between the EC-SOD genotypes in the larger lesions seen after 3 months on the diet or after 8 months on normal chow. Despite smaller or equal lesions in the EC-SOD-null mice, their cholesterol levels were somewhat higher. Also, on a wild-type background, there were no effects produced by the absence or presence of EC-SOD on atherogenic diet-induced aortic root lesions. The urinary excretion of the lipid peroxidation biomarker 8-isoprostaglandin F(2alpha) was related to the rates of atherogenesis in the mice but was not influenced by the EC-SOD genotype. Likewise, the EC-SOD status had no effect on the staining for oxidized low density lipoprotein epitopes in aortic root sections. Our findings suggest that EC-SOD has little influence on atherogenesis in mice.
authors.affiliation: Department of Medical Biosciences, Clinical Chemistry, Umeå University Hospital, Umeå, Sweden.
authors.forename: M L
authors.initials: ML
authors.lastname: Sentman
authors.forename: T
authors.initials: T
authors.lastname: Brännström
authors.forename: S
authors.initials: S
authors.lastname: Westerlund
authors.forename: M O
authors.initials: MO
authors.lastname: Laukkanen
authors.forename: S
authors.initials: S
authors.lastname: Ylä-Herttuala
authors.forename: S
authors.initials: S
authors.lastname: Basu
authors.forename: S L
authors.initials: SL
authors.lastname: Marklund
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000473:pathology; D001057:Apolipoproteins E / Q000235:genetics; D001161:Arteriosclerosis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D002784:Cholesterol / Q000097:blood; D004036:Diet, Atherogenic; D015237:Dinoprost / Q000031:analogs & derivatives / Q000652:urine; D028441:F2-Isoprostanes; D005260:Female; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D013482:Superoxide Dismutase / Q000235:genetics* / Q000502:physiology*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D001057:Apolipoproteins E; D028441:F2-Isoprostanes; D008077:Lipoproteins, LDL; D017392:Thiobarbituric Acid Reactive Substances; C099252:oxidized low density lipoprotein; C075750:8-epi-prostaglandin F2alpha; D002784:Cholesterol; D015237:Dinoprost; D013482:Superoxide Dismutase