Testicular toxicity of Aroclor 1254 in selenium-deficient and selenium-supplemented rats; [Toksičnost Aroclora 1254 u testisa štakora s manjkom selena i u onih na nadomjesnom selenu]

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Özet

Aroclor 1254 (A1254) is a mixture of polychlorinated biphenyl (PCB) congeners known to induce testicular toxicity through oxidative stress, apoptosis, and hormonal disruption. Selenium (Se), an essential trace element for male reproduction, contributes to antioxidant defence, DNA repair, and spermatogenesis. Given the worldwide prevalence of Se deficiency and its potential impact on reproductive health, this study investigated the effects of A1254 exposure on testicular function in Sprague-Dawley rats with different Se status. Rats assigned to the Se-deficient group were receiving a ≤0.05 mg/kg Se diet, while those assigned to the Se-supplemented group were receiving 1 mg/kg Se for five weeks. A1254-treated groups were receiving 10 mg/kg/day of A1254 by oral gavage for 15 consecutive days. A1254 exposure caused significant reductions in testis weight, sperm count, motility, and plasma testosterone levels, accompanied by extensive germ cell apoptosis and enhanced lipid and protein oxidation. Total antioxidant capacity also dropped significantly, confirming redox imbalance in A1254-exposed testes. These adverse effects were substantially exacerbated in the Se-deficient group, whereas Se supplementation ameliorated but did not fully prevent histological and biochemical changes induced by A1254. Our findings demonstrate that Se plays a crucial protective role against PCB-associated testicular injury, primarily by mitigating oxidative stress and apoptotic pathways. However, Se supplementation alone may not completely counteract the reproductive toxicity caused by persistent environmental contaminants such as A1254. © 2026 Pınar Erkekoğlu et al., published by Institute for Medical Research and Occupational Health.

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https://rdlopen.rawdatalibrary.net/r/ebyu/10053Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.2478/aiht-2026-77-4027Yayıncı resmi DOI adresi
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AlanDeğerDil
dc.contributor.authorErkekoğlu, Pınar
dc.contributor.authorBalcı-Özyurt, Aylin
dc.contributor.authorZeybek, Naciye Dilara
dc.contributor.authorTezel-Yalçın, Hülya
dc.contributor.authorYaman, Ünzile
dc.contributor.authorYildiztekin, Gizem
dc.contributor.authorAydın-Dilsiz, Sevtap
dc.contributor.authorKızılgün, Murat
dc.contributor.authorİşcan, Evin
dc.contributor.authorBatur, Tuğçe
dc.contributor.authorÖztürk, Mehmet
dc.contributor.authorEdebal, Oğuz Han
dc.contributor.authorBaşaran, Nurşen
dc.contributor.authorKoçer-Gumusel, Belma
dc.date.accessioned2026-10-18T20:25:17.645177135Z
dc.date.available2026-10-18T20:25:17.645177135Z
dc.date.issued2026
dc.description.abstractAroclor 1254 (A1254) is a mixture of polychlorinated biphenyl (PCB) congeners known to induce testicular toxicity through oxidative stress, apoptosis, and hormonal disruption. Selenium (Se), an essential trace element for male reproduction, contributes to antioxidant defence, DNA repair, and spermatogenesis. Given the worldwide prevalence of Se deficiency and its potential impact on reproductive health, this study investigated the effects of A1254 exposure on testicular function in Sprague-Dawley rats with different Se status. Rats assigned to the Se-deficient group were receiving a ≤0.05 mg/kg Se diet, while those assigned to the Se-supplemented group were receiving 1 mg/kg Se for five weeks. A1254-treated groups were receiving 10 mg/kg/day of A1254 by oral gavage for 15 consecutive days. A1254 exposure caused significant reductions in testis weight, sperm count, motility, and plasma testosterone levels, accompanied by extensive germ cell apoptosis and enhanced lipid and protein oxidation. Total antioxidant capacity also dropped significantly, confirming redox imbalance in A1254-exposed testes. These adverse effects were substantially exacerbated in the Se-deficient group, whereas Se supplementation ameliorated but did not fully prevent histological and biochemical changes induced by A1254. Our findings demonstrate that Se plays a crucial protective role against PCB-associated testicular injury, primarily by mitigating oxidative stress and apoptotic pathways. However, Se supplementation alone may not completely counteract the reproductive toxicity caused by persistent environmental contaminants such as A1254. © 2026 Pınar Erkekoğlu et al., published by Institute for Medical Research and Occupational Health.
dc.description.sponsorshipThis work was supported by Hacettepe University Scientific Research Unit Research Project (grant No. 012 D12 301 003).
dc.identifier.doi10.2478/aiht-2026-77-4027
dc.identifier.endpage113
dc.identifier.issn0004-1254
dc.identifier.issue2
dc.identifier.pmcidPMC13331366
dc.identifier.pmid42398009
dc.identifier.scopus2-s2.0-105044034593
dc.identifier.startpage102
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/10053
dc.identifier.volume77
dc.language.isoen
dc.publisherParadigm Publishing Services
dc.relation.ispartofArhiv za Higijenu Rada i Toksikologiju
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectapoptosis
dc.subjectoxidative stress
dc.subjectpolychlorinated biphenyls
dc.subjectSe
dc.subjectsperm
dc.subjectAnimals
dc.subjectChlorodiphenyl (54% Chlorine)
dc.subjectDietary Supplements
dc.subjectMale
dc.subjectRats
dc.subjectRats, Sprague-Dawley
dc.subjectSelenium
dc.subjectTestis
dc.subjectaroclor 1254
dc.subjectcaspase 3
dc.subjectcaspase 8
dc.subjectestradiol
dc.subjectprotein p21
dc.subjectprotein p53
dc.subjecttestosterone
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectbiochemical composition
dc.subjectbody weight gain
dc.subjectcell cycle checkpoint
dc.subjectcontrolled study
dc.subjectenzyme activity
dc.titleTesticular toxicity of Aroclor 1254 in selenium-deficient and selenium-supplemented rats; [Toksičnost Aroclora 1254 u testisa štakora s manjkom selena i u onih na nadomjesnom selenu]
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus0
rdl.departmentErzincan Binali Yıldırım University Faculty of Pharmacy, Department of Pharmaceutical Toxicology, Erzincan, Turkey.
rdl.oa.statusgold
rdl.source.indexSCOPUS
rdl.source.indexPUBMED