{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T18:48:11Z","timestamp":1776278891829,"version":"3.50.1"},"reference-count":46,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2017,3,13]],"date-time":"2017-03-13T00:00:00Z","timestamp":1489363200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"Deanship of research at Jordan University of Science and Technology","award":["292\/2014"],"award-info":[{"award-number":["292\/2014"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cardiovascular Therapeutics"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Diabetes mellitus (<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>) is linked to cardiovascular diseases development and progression. Aldosterone contributes to cardiac oxidative stress and remodeling.<\/jats:p><\/jats:sec><jats:sec><jats:title>Aim<\/jats:title><jats:p>To evaluate the impact of spironolactone (an aldosterone antagonist) on markers of myocardial redox status in a rat model of streptozotocin (<jats:styled-content style=\"fixed-case\">STZ<\/jats:styled-content>)\u2010induced <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Method<\/jats:title><jats:p>Adult Sprague Dawley rats were randomized into four groups; controls, spironolactone\u2010treated rats (Spir), diabetic rats (<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>), and diabetic rats treated with spironolactone (<jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>+Spir) for 4\u00a0weeks. Blood pressure and cardiac levels of aldosterone and oxidants\/antioxidants were measured.<\/jats:p><\/jats:sec><jats:sec><jats:title>Result<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">STZ<\/jats:styled-content><jats:bold>\u2010<\/jats:bold>induced <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> but did not cause hypertension or dyslipidemia in either spironolactone\u2010treated or spironolactone\u2010untreated rats. Aldosterone and aldosterone synthase levels were increased in both the <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>+Spir groups compared to control. In parallel, total nitrite and nitrotyrosine levels were increased and vitamin E antioxidant levels were reduced in the <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> group. Spironolactone use reduced cardiac total nitrite levels and improved vitamin E levels. Glutathione reductase\/peroxidase activities were increased in the <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content>+Spir groups without changes in the ratio of reduced to oxidized form of glutathione. Superoxide dismutase (<jats:styled-content style=\"fixed-case\">SOD<\/jats:styled-content>) and catalase activities were increased in the <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> group. Lipid peroxidation products were similar among the groups.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The increase in total nitrite\/nitrotyrosine in <jats:styled-content style=\"fixed-case\">DM<\/jats:styled-content> promoted significant compensatory increases in antioxidant activities of <jats:styled-content style=\"fixed-case\">SOD<\/jats:styled-content>, catalase and glutathione peroxidase\/reductase probably to prevent cardiac oxidative damage. 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