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Forty-eight oophorectomized rabbits were divided into 5 groups and fed the following diets for 10 weeks: group 1, a regular rabbit diet plus 1% cholesterol (a high-cholesterol diet [HCD]); group 2, an HCD plus 0.3% DHEA; group 3, an HCD plus 0.3% DHEA and fadrozole (2.0 mg \u00b7 kg\n            <jats:sup>\u22121<\/jats:sup>\n            \u00b7 d\n            <jats:sup>\u22121<\/jats:sup>\n            ), a specific aromatase inhibitor; group 4, an HCD plus 17\u03b2-estradiol (20 \u03bcg \u00b7 kg\n            <jats:sup>\u22121<\/jats:sup>\n            \u00b7 d\n            <jats:sup>\u22121<\/jats:sup>\n            ); and group 5, a regular diet. Atherosclerotic lesions, lipid deposition in aortic vessels, and basal and stimulated NO release were measured in the aforementioned groups of rabbits. NO release was measured by using an NO-selective electrode as well as by measuring vascular responses and the plasma NO metabolites nitrite and nitrate. The plasma total cholesterol level was increased, but there were no significant differences in lipid profile in the 4 groups of rabbits that were fed the HCD. The area occupied by atherosclerosis in the thoracic aorta was diminished by \u224860% in the DHEA-treated rabbits (group 2) compared with the HCD group of rabbits (group 1); there was a corresponding 80% decrease in the estradiol group (group 4) but only a 30% decrease in the DHEA plus fadrozole group (group 3). In the aortas of rabbits from groups 1 and 3, the acetylcholine-induced and tone-related basal NO-mediated relaxations were diminished compared with those of the controls (group 5). However, these relaxations were restored in the aortas of group 2 and 4 rabbits, and an increase in NO release was observed in groups 2 and 4 compared with groups 1 and 3, as measured by an NO-selective electrode. Injection of neither solvent (20% ethanol\/distilled water) nor fadrozole significantly affected the atherosclerotic area or the NO-related responses described above. We conclude that \u224850% of the total antiatherosclerotic effect of DHEA was achieved through the conversion of DHEA to estrogen. NO may also play a role in the antiatherosclerotic effect of DHEA and 17\u03b2-estradiol.\n          <\/jats:p>","DOI":"10.1161\/01.atv.20.3.782","type":"journal-article","created":{"date-parts":[[2011,6,17]],"date-time":"2011-06-17T19:44:19Z","timestamp":1308339859000},"page":"782-792","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":82,"title":["Dehydroepiandrosterone Retards Atherosclerosis Formation Through Its Conversion to Estrogen"],"prefix":"10.1161","volume":"20","author":[{"given":"Toshio","family":"Hayashi","sequence":"first","affiliation":[{"name":"From the Department of Geriatrics, Nagoya University School of Medicine, Nagoya, Japan."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Teiji","family":"Esaki","sequence":"additional","affiliation":[{"name":"From the Department of Geriatrics, Nagoya University School of Medicine, Nagoya, 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