title: Hydroxytyrosol administration enhances atherosclerotic lesion development in apo E deficient mice.
abstract: Hydroxytyrosol is a phenol found in olive oil. To verify the effect of hydroxytyrosol on the development of atherosclerosis, two groups of apo E deficient male mice on a standard chow diet were used: the control group receiving only water, and the second group an aqueous solution of hydroxytyrosol in order to provide a dose of 10 mg/kg/day to each mouse. This treatment was maintained for 10 weeks. At the moment of sacrifice, blood was drawn and heart removed. Plasma lipids, apolipoproteins and monocyte Mac-1 expression were assayed as well as aortic atherosclerotic areas in both groups. Data showed no significant changes in HDL cholesterol, paraoxonase, apolipoprotein B or triglyceride levels. However, hydroxytyrosol administration decreased apolipoprotein A-I and increased total cholesterol, atherosclerotic lesion areas and circulating monocytes expressing Mac-1. The latter was highly correlated with lesion areas (r = 0.65, P < 0.01). These results indicate that administration of hydroxytyrosol in low cholesterol diets increases atherosclerotic lesion associated with the degree of monocyte activation and remodelling of plasma lipoproteins. Our data supports the concept that phenolic-enriched products, out of the original matrix, could be not only non useful but also harmful. Our results suggest that the formulation of possible functional foods should approximate as much as possible the natural environment in which active molecules are found.
authors.affiliation: Departamento de Bioquímica y Biología Molecular y Celular, Facultad de Veterinaria, Universidad de Zaragoza.
authors.forename: Sergio
authors.initials: S
authors.lastname: Acín
authors.forename: María A
authors.initials: MA
authors.lastname: Navarro
authors.forename: José M
authors.initials: JM
authors.lastname: Arbonés-Mainar
authors.forename: Natalia
authors.initials: N
authors.lastname: Guillén
authors.forename: Alfonso J
authors.initials: AJ
authors.lastname: Sarría
authors.forename: Ricardo
authors.initials: R
authors.lastname: Carnicer
authors.forename: Joaquín C
authors.initials: JC
authors.lastname: Surra
authors.forename: Israel
authors.initials: I
authors.lastname: Orman
authors.forename: Jose C
authors.initials: JC
authors.lastname: Segovia
authors.forename: Rafael de la
authors.initials: Rde L
authors.lastname: Torre
authors.forename: María-Isabel
authors.initials: MI
authors.lastname: Covas
authors.forename: Juan
authors.initials: J
authors.lastname: Fernández-Bolaños
authors.forename: Valentina
authors.initials: V
authors.lastname: Ruiz-Gutiérrez
authors.forename: Jesús
authors.initials: J
authors.lastname: Osada
mesh_terms: D000818:Animals; D016632:Apolipoprotein A-I / Q000097:blood*; D001055:Apolipoproteins B / Q000097:blood; D001057:Apolipoproteins E / Q000172:deficiency*; D043303:Aryldialkylphosphatase / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D003324:Coronary Artery Disease / Q000139:chemically induced / Q000473:pathology*; D017931:DNA Primers; D016177:Macrophage-1 Antigen / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D009000:Monocytes / Q000378:metabolism; D010626:Phenylethyl Alcohol / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000633:toxicity / Q000652:urine; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014280:Triglycerides / Q000097:blood
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D017931:DNA Primers; D016177:Macrophage-1 Antigen; D014280:Triglycerides; C005975:3,4-dihydroxyphenylethanol; D043303:Aryldialkylphosphatase; D010626:Phenylethyl Alcohol