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
Arhiv za Higijenu Rada i Toksikologiju, cilt.77, sa.2, ss.102-113, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 77 Sayı: 2
- Basım Tarihi: 2026
- Doi Numarası: 10.2478/aiht-2026-77-4027
- Dergi Adı: Arhiv za Higijenu Rada i Toksikologiju
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, Greenfile, MEDLINE, SportDiscus, Directory of Open Access Journals, Academic Search Ultimate (EBSCO), East & Central Europe Database (ProQuest), Natural Science Collection (ProQuest), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest)
- Sayfa Sayıları: ss.102-113
- Anahtar Kelimeler: apoptosis, oxidative stress, polychlorinated biphenyls, Se, sperm
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- Erzincan Binali Yıldırım Üniversitesi Adresli: Evet
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.