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Forty male Wistar albino rats were randomly allocated to Control, Ch, AFB\n                    <jats:sub>1<\/jats:sub>\n                    , and Ch+AFB\n                    <jats:sub>1<\/jats:sub>\n                    groups. Chrysin (25\u00a0mg\/kg BW \/day) was administered orally for 11 days, while AFB\n                    <jats:sub>1<\/jats:sub>\n                    (0.5\u00a0mg\/kg BW \/day) for 7 days. AFB\n                    <jats:sub>1<\/jats:sub>\n                    exposure induced pronounced hepato-renal injury and histopathological alterations. At the molecular level, it caused excessive oxidative stress, evidenced by glutathione depletion and elevated malondialdehyde and 8-hydroxy-2\u2032-deoxyguanosine levels, indicating lipid peroxidation and oxidative DNA damage. This redox imbalance activated inflammatory signaling, reflected by increased NF-\u03baB p65 and TNF-\u03b1, alongside dysregulated Sirt-1 expression, suggesting disruption of redox-sensitive transcriptional control. Persistent oxidative and inflammatory stress further promoted mitochondrial apoptosis, as indicated by upregulated Caspase-3 and Caspase-9, and triggered compensatory proliferation, demonstrated by elevated PCNA and Ki-67 levels. Co-administration of Chrysin mitigated these biochemical and molecular alterations by restoring antioxidant defenses, suppressing NF-\u03baB\u2013mediated inflammation via modulation of the Sirt-1\/NF-\u03baB axis, and attenuating apoptotic and proliferative signaling. These molecular improvements were accompanied by preservation of hepatic and renal histoarchitecture. Although the animals exhibited subclinical biochemical and histological stress, no overt clinical illness was observed during the study. In conclusion, AFB\n                    <jats:sub>1<\/jats:sub>\n                    -induced hepato-renal toxicity is driven by interconnected oxidative, inflammatory, and apoptotic mechanisms. Chrysin provides multi-level protection by modulating these pathways, highlighting its potential as a protective agent against mycotoxin-induced toxic injury.\n                  <\/jats:p>","DOI":"10.1007\/s12550-026-00655-z","type":"journal-article","created":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T03:58:05Z","timestamp":1781150285000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Redox-sensitive and inflammatory pathway modulation by Chrysin confers protection against aflatoxin B1\u2013induced hepato-renal damage"],"prefix":"10.1007","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3954-8578","authenticated-orcid":false,"given":"Esra","family":"Zeybek","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5227-1289","authenticated-orcid":false,"given":"As\u0131m","family":"Kart","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1835-1082","authenticated-orcid":false,"given":"\u00d6zlem","family":"\u00d6zmen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,6,11]]},"reference":[{"key":"655_CR1","doi-asserted-by":"publisher","first-page":"144781","DOI":"10.1016\/j.scitotenv.2020.144781","volume":"768","author":"MM Abdel-Daim","year":"2021","unstructured":"Abdel-Daim MM, Abdeen A, Jalouli M, Abdelkader A, Megahed A, Alkahtane A, Aleya L (2021) Fucoidan supplementation modulates hepato-renal oxidative stress and DNA damage induced by aflatoxin B1 intoxication in rats. 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