Erkekoğlu, Pınar; Balcı-Özyurt, Aylin; Zeybek, Naciye Dilara; Tezel-Yalçın, Hülya; Yaman, Ünzile; Yildiztekin, Gizem; Aydın-Dilsiz, Sevtap; Kızılgün, Murat; İşcan, Evin; Batur, Tuğçe

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.

Zeybek, Naciye Dilara; Sur, Ünzile; Oflaz, Ofcan; Erkekoǧlu, Plnar; Balcl, Aylin; Özkemahll, Gizem; Aşçl, Ali; Klzllgün, Murat; Edebal, Oǧuz Han; Koçer-Gümüşel, Belma

Aroclor 1254 (A1254), a mixture of polychlorinated biphenyls, exerts hepatic, renal, and reproductive toxicity in rodents. This study aimed to determine a protective role of selenium on histopathological changes, oxidative stress, and apoptosis caused by A1254 in rat kidney. It included a control group, which received regular diet containing 0.15 mg/kg Se (C), a Se-supplemented group (SeS) receiving 1 mg/kg Se, a Se-deficient group (SeD) receiving Se-deficient diet of ≤0.05 mg/kg Se, an A1254-treated group (A) receiving 10 mg/kg of Aroclor 1254 and regular diet, an A1254-treated group receiving Se-supplementation (ASeS), and an A1254-treated group receiving Se-deficient diet (ASeD). Treatments lasted 15 days. After 24 h of the last dose of A1254, the animals were decapitated under anaesthesia and their renal antioxidant enzyme activities, lipid peroxidation (LP), glutathione, protein oxidation, and total antioxidant capacity levels measured. Histopathological changes were evaluated by light and electron microscopy. Apoptosis was detected with the TUNEL assay. Kidney weights, CAT activities, and GSH levels decreased significantly in all A1254-treated groups. Renal atrophic changes and higher apoptotic cell counts were observed in the A and ASeD groups. Both groups also showed a significant drop in GPx1 activities (A-34.92 % and ASeD-86.46 %) and rise in LP (A-30.45 % and ASeD-20.44 %) vs control. In contrast, LP levels and apoptotic cell counts were significantly lower in the ASeS group vs the A group. Histopathological changes and renal apoptosis were particularly visible in the ASeD group. Our findings suggest that selenium supplementation provides partial protection against renal toxicity of Aroclor 1254.