title: Systemic markers of the redox balance and apolipoprotein E polymorphism in atherosclerosis: the relevance for an integrated study.
abstract: Prospective studies have demonstrated that an imbalance between oxidative damage and antioxidative protection can play a role in the development and progression of atherosclerosis. Also, genotypes with the apolipoprotein E epsilon4 allele have been associated with an increase risk for this pathology. Based on this knowledge, the aim of this study was to evaluate indicators of the redox balance, trace elements, and apolipoprotein E allelic profile in subjects from the Lisbon population with clinically stable atherosclerosis, at risk for atherosclerotic events, and in healthy subjects for comparison. The activities of superoxide dismutase in erythrocytes and glutathione peroxidase in whole blood, plasma total thiols, and serum ceruloplasmin were kept unchanged among the three groups. Serum alpha- tocopherol was increased in atherosclerotic patients. Total malondialdehyde in serum and protein carbonyls in plasma, which are indicators of lipid and protein oxidative damage, respectively, reached their highest values in risk subjects. The concentrations of potassium and calcium, in plasma and in blood cells, were slightly elevated in patients and might reflect an electrolytic imbalance. Regarding the apolipoprotein E polymorphism, atherosclerotic patients had an increased incidence of the high-risk genotypes for atherogenesis (epsilon3/epsilon4 and epsilon4/epsilon4). A multivariate model applied to the general population using most of the parameters clearly separated the three groups at study (i.e., the healthy group from the steady-state group of risk disease and from the atherosclerotic one). As shown by us, the usefulness of biochemical and complementary genetic markers is warranted for a better knowledge on atherosclerosis molecular basis.
authors.affiliation: Centro de Biologia Ambiental and Departamento de Biologia Animal, Faculdade de Ciências, Universidade de Lisboa, 1749-016 Lisboa, Portugal.
authors.forename: Paula A
authors.initials: PA
authors.lastname: Lopes
authors.forename: Patrícia
authors.initials: P
authors.lastname: Napoleão
authors.forename: Teresa
authors.initials: T
authors.lastname: Pinheiro
authors.forename: Fátima
authors.initials: F
authors.lastname: Ceia
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Steghens
authors.forename: M Leoner
authors.initials: ML
authors.lastname: Pavão
authors.forename: M Cristina
authors.initials: MC
authors.lastname: Santos
authors.forename: Ana M
authors.initials: AM
authors.lastname: Viegas-Crespo
mesh_terms: D000328:Adult; D000368:Aged; D001057:Apolipoproteins E / Q000235:genetics / Q000378:metabolism*; D050197:Atherosclerosis / Q000235:genetics / Q000378:metabolism*; D002118:Calcium / Q000097:blood; D016022:Case-Control Studies; D005838:Genotype; D005979:Glutathione Peroxidase / Q000097:blood; D006801:Humans; D015227:Lipid Peroxidation; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D010084:Oxidation-Reduction; D011110:Polymorphism, Genetic; D011188:Potassium / Q000097:blood; D013438:Sulfhydryl Compounds / Q000097:blood; D013482:Superoxide Dismutase / Q000378:metabolism; D024502:alpha-Tocopherol / Q000097:blood
chemical_list: D001057:Apolipoproteins E; D013438:Sulfhydryl Compounds; D008315:Malondialdehyde; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D024502:alpha-Tocopherol; D011188:Potassium; D002118:Calcium