{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T07:25:56Z","timestamp":1786951556194,"version":"build-2736575974"},"reference-count":42,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T00:00:00Z","timestamp":1784592000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T00:00:00Z","timestamp":1784592000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Biochem &amp;amp; Molecular Tox"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Excessive alcohol consumption causes significant cardio\u2010hepatic damage. This study investigated the effects of standard (10\u2009mg\/kg) and high (40\u2009mg\/kg) doses of atorvastatin on fibrosis, hypertrophy, apoptosis, inflammation, oxidative stress, mitochondrial\u2010mediated apoptotic pathways, and thiol\/disulfide balance in alcohol\u2010induced heart and liver injury. Forty Sprague\u2010Dawley rats were divided into five groups (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20098; 4 male\/4 female): Control (CONT), ALCOHOL (2.5\u2009g\/kg 20% ethanol i.p.\/28 days), ATOR (10\u2009mg\/kg o.g.\/28 days), ALCOHOL\u2009+\u2009ATOR (10\u2009mg\/kg o.g.\/28 days) and ALCOHOL+\u2009hATOR (40\u2009mg\/kg o.g.\/28 days). Histopathologically, alcohol caused cardiac myocyte dilation, vacuolization, inflammation, and hepatic cord disruption. While standard ATOR partially improved tissue architecture (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.001), the ALCOHOL+\u2009hATOR group showed the lowest severity. Alcohol exposure significantly increased apoptosis (Caspase\u20103, M30, M65), oxidative stress (TOS, OSI, MDA), ischemia (IMA), and inflammatory cytokines (IL\u20101\u03b2, TNF\u2010\u03b1, HsCRP, Endothelin\u20101) across serum, heart, and liver samples, while decreasing TAS, total thiol, and native thiol levels (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.001 for all vs. CONT). Conversely, high\u2010dose atorvastatin (ALCOHOL\u2009+\u2009hATOR) significantly reversed alcohol\u2010induced toxicity by decreasing Caspase\u20103, M30, M65, TOS, OSI, MDA, TNF\u2010\u03b1, HsCRP, Endothelin\u20101, and disulfide levels, while significantly restoring TAS, total thiol, and native thiol levels (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.001 vs. ALCOHOL). TAS was significantly higher in the ALCOHOL+hATOR group than the ALCOHOL\u2009+\u2009ATOR group (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.001). Despite marked improvements by hATOR, OSI, TOS, IL\u20101\u03b2, and HsCRP levels remained higher than CONT (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.001). High\u2010dose atorvastatin (40\u2009mg\/kg) exerts robust pleiotropic, anti\u2010apoptotic, and antioxidant cytoprotection. By preserving thiol\u2010disulfide homeostasis and limiting inflammation, high\u2010dose atorvastatin effectively mitigates alcohol\u2010induced subchronic cardiac and hepatic injury.\n                  <\/jats:p>","DOI":"10.1002\/jbt.71036","type":"journal-article","created":{"date-parts":[[2026,7,21]],"date-time":"2026-07-21T13:43:46Z","timestamp":1784641426000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Atorvastatin Reduces Alcohol\u2010Related Cardiac and Liver Tissue Damage, Oxidative Stress, Inflammation, Apoptosis, and Thiol\u2010Disulfide Imbalance in Rats"],"prefix":"10.1002","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5226-6730","authenticated-orcid":false,"given":"Cumaali","family":"Demirtas","sequence":"first","affiliation":[{"name":"Hamidiye Health Sciences Institute University of Health Sciences Istanbul Turkiye"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3524-5396","authenticated-orcid":false,"given":"\u015eahhan","family":"K\u0131l\u0131\u00e7","sequence":"additional","affiliation":[{"name":"Cardiology Department of \u00c7orlu State Hospital Tekirda\u011f Turkiye"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4544-9584","authenticated-orcid":false,"given":"Mert","family":"Babao\u011flu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Sultan II. Abdulhamid Training and Research Hospital University of Health Sciences Istanbul Turkiye"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3709-2506","authenticated-orcid":false,"given":"S\u00fcha","family":"Asal","sequence":"additional","affiliation":[{"name":"Cardiology Department of \u00c7orlu State Hospital Tekirda\u011f Turkiye"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-3847-1421","authenticated-orcid":false,"given":"Elif G\u00f6k\u00e7e","family":"Tenekeci","sequence":"additional","affiliation":[{"name":"G\u00fclhane Health Sciences Institute University of Health Sciences Ankara Turkiye"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3706-5193","authenticated-orcid":false,"given":"Hakan","family":"Beyazta\u015f","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Hamidiye Faculty of Medicine University of Health 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