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This work aimed to study the impact of methionine\u2010induced hyperhomocysteinemia (<jats:styled-content style=\"fixed-case\">HH<\/jats:styled-content>cy) on two major antiatherogenic functions of <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>, namely their capacity to prevent <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content> oxidation and induce in vivo macrophage\u2010specific reverse cholesterol transport.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and results<\/jats:title><jats:p>Methionine\u2010induced <jats:styled-content style=\"fixed-case\">HH<\/jats:styled-content>cy in mice resulted in an approximately 20% decreased concentration of <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010cholesterol and <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content> main protein component, apolipoprotein <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>. The <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content> potential to resist oxidation as well as to prevent <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content> oxidative modification was impaired in hyperhomocysteinemic mice. Activities of paraoxonase\u20101 and platelet activation factor acetylhydrolase, two of the main <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content>\u2010associated enzymes with antioxidant activity, were reduced. The ability of <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content> to efflux cholesterol from macrophages was decreased in hyperhomocysteinemic mice; however, the in vivo macrophage\u2010specific reverse cholesterol transport measured as the output of labeled cholesterol into feces did not significantly differ between groups.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our data indicate that the <jats:styled-content style=\"fixed-case\">HDL<\/jats:styled-content> from methionine\u2010induced hyperhomocysteinemic mice was more prone to oxidation and displayed lower capacity to protect <jats:styled-content style=\"fixed-case\">LDL<\/jats:styled-content> against oxidative modification than that of control mice, highlighting a mechanism by which a diet\u2010induced <jats:styled-content style=\"fixed-case\">HH<\/jats:styled-content>cy may facilitate progression of atherosclerosis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/mnfr.201300133","type":"journal-article","created":{"date-parts":[[2013,6,10]],"date-time":"2013-06-10T11:24:44Z","timestamp":1370863484000},"page":"1814-1824","source":"Crossref","is-referenced-by-count":19,"title":["Methionine\u2010induced hyperhomocysteinemia impairs the antioxidant ability of high\u2010density lipoproteins without reducing in vivo macrophage\u2010specific reverse cholesterol transport"],"prefix":"10.1002","volume":"57","author":[{"given":"Josep","family":"Julve","sequence":"first","affiliation":[{"name":"Institut d'Investigacions Biom\u00e8diques Sant Pau (IIB\u2010Sant Pau)  Barcelona Spain"},{"name":"CIBER de Diabetes y Enfermedades Metab\u00f3licas Asociadas  CIBERDEM Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joan C.","family":"Escol\u00e0\u2010Gil","sequence":"additional","affiliation":[{"name":"Institut d'Investigacions Biom\u00e8diques Sant Pau (IIB\u2010Sant Pau)  Barcelona 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