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For this purpose, rats were divided into four groups: Control, CHR, HgCl\n                    <jats:sub>2<\/jats:sub>\n                    and HgCl\n                    <jats:sub>2<\/jats:sub>\n                    \u2009+\u2009CHR. HgCl\n                    <jats:sub>2<\/jats:sub>\n                    was administered intraperitoneally at a dose of 1.23\u00a0mg\/kg, and CHR was administered orally at a dose of 50\u00a0mg\/kg for 7 days. Biochemical, molecular and immunohistochemical analyses were performed to determine the effect of treatment-mediated changes in the testicular tissue. Based on the results obtained in testicular tissue, administration of HgCl\n                    <jats:sub>2<\/jats:sub>\n                    was observed to lower antioxidant markers, elevate malondialdehyde (MDA) levels, and increase inflammatory marker expression in rat testicular tissue. It also led to reduced testosterone levels. Additionally, there was a decrease in the expression of antiapoptotic B-cell lymphoma 2 (Bcl-2) an apoptosis marker while the levels of Caspase-3 and Bcl-2-associated X protein (Bax) were found to be higher. The endoplasmic reticulum stress marker protein kinase R-like ER kinase (PERK) and the autophagy marker Beclin-1 showed strong immunoreactivity. Additionally, HgCl\n                    <jats:sub>2<\/jats:sub>\n                    \u2009+\u2009CHR treatment were found to significantly reduce oxidative stress, inflammation, apoptosis, endoplasmic reticulum stress and autophagy processes in testicular tissue. In conclusion, HgCl\n                    <jats:sub>2<\/jats:sub>\n                    administration to rats caused testicular tissue damage compared to the other groups, but CHR treatment alleviated this damage. Overall, this demonstrates the potential ameliorative mechanisms of CHR as a possible agent for HgCl\n                    <jats:sub>2<\/jats:sub>\n                    -induced testicular damage.\n                  <\/jats:p>","DOI":"10.1007\/s12011-026-04993-y","type":"journal-article","created":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T08:27:58Z","timestamp":1768897678000},"page":"2052-2064","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Protective Role of Chrysin against Mercury Chloride-Induced Testicular Damage via Oxidative Stress, Inflammation, Apoptosis, Endoplasmic Reticulum Stress, and Autophagy Pathways"],"prefix":"10.1007","volume":"204","author":[{"given":"Serpil","family":"Ayg\u00f6rmez","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mustafa","family":"Makav","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ebru","family":"Karada\u011f Sar\u0131","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elif","family":"Dalk\u0131l\u0131n\u00e7","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hamit","family":"Uslu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"\u015eaban","family":"Mara\u015fl\u0131","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,1,20]]},"reference":[{"key":"4993_CR1","doi-asserted-by":"crossref","first-page":"7273","DOI":"10.1007\/s00210-024-03585-8","volume":"398","author":"MP Sampada","year":"2025","unstructured":"Sampada MP, David M (2025) Mercuric chloride induced reproductive toxicity associated with oxidative damage in male Wistar albino rat, rattus norvegicus. 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