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<p>Finasteride (FNS), a widely used 5α-reductase inhibitor, is associated with reproductive toxicity. However, the molecular mechanisms concerning the blood-testis barrier (BTB) integrity and inflammatory signaling pathways remain unclear. This study evaluated whether zinc oxide nanoparticles (ZnO NPs) were associated with attenuation of FNS-induced testicular injury in rats. Thirty-five male Sprague–Dawley rats were allocated to Control, FNS (5&#xa0;mg/kg), ZnO NP (30&#xa0;mg/kg), FNS + ZnO NP 15&#xa0;mg/kg, and FNS + ZnO NP 30&#xa0;mg/kg groups and treated orally for 28 days. Sperm quality, reproductive organ weights, serum testosterone and oxidative stress index (OSI), testicular histopathology, junctional-protein immunostaining, RT-qPCR, and Western blot analyses were evaluated. Compared with Control, FNS reduced sperm motility and concentration and increased dead sperm, abnormal morphology, and DNA damage. FNS also increased NF-κB and caspase-3 protein abundance and decreased BCL-2, PI3K, and NRF2. Co-treatment, particularly at 30&#xa0;mg/kg, was associated with improved sperm motility and concentration, a lower dead sperm rate, reduced histopathological damage, lower NF-κB and caspase-3 abundance, and improvement in selected junctional-protein staining relative to FNS alone. However, abnormal sperm morphology and DNA damage at 30&#xa0;mg/kg were not significantly different from the FNS group, and PI3K and NRF2 were not significantly restored. Serum testosterone did not differ among groups, whereas OSI showed an overall group effect (<i>p</i> = 0.007). Tissue-specific oxidative stress markers and pathway phosphorylation were not assessed. These findings provide preliminary, associative evidence that ZnO NPs may partially attenuate FNS-associated testicular injury; they do not establish NF-κB/STAT3 signaling or oxidative stress as causal mechanisms.</p>

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Preliminary Associative Evidence on Zinc Oxide Nanoparticle Co-administration in Finasteride-Induced Testicular Toxicity: Inflammatory Markers and Blood–Testis Barrier-Related Proteins in Rats

  • 期刊论文

  • 发表日期：

    2026年7月30日

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  • Ibrahim Enes Ergen,
  • Serkan Ali Akarsu,
  • Gökhan Doğukan Akarsu,
  • Adem Kara,
  • Elif Erbaş,
  • Gamze Uçak,
  • Mehmet Akif Aydın,
  • Hakan Serin,
  • Cemil Bayram,
  • Beyza Nur Aydemir,
  • Seviye Olgun

摘要

Finasteride (FNS), a widely used 5α-reductase inhibitor, is associated with reproductive toxicity. However, the molecular mechanisms concerning the blood-testis barrier (BTB) integrity and inflammatory signaling pathways remain unclear. This study evaluated whether zinc oxide nanoparticles (ZnO NPs) were associated with attenuation of FNS-induced testicular injury in rats. Thirty-five male Sprague–Dawley rats were allocated to Control, FNS (5 mg/kg), ZnO NP (30 mg/kg), FNS + ZnO NP 15 mg/kg, and FNS + ZnO NP 30 mg/kg groups and treated orally for 28 days. Sperm quality, reproductive organ weights, serum testosterone and oxidative stress index (OSI), testicular histopathology, junctional-protein immunostaining, RT-qPCR, and Western blot analyses were evaluated. Compared with Control, FNS reduced sperm motility and concentration and increased dead sperm, abnormal morphology, and DNA damage. FNS also increased NF-κB and caspase-3 protein abundance and decreased BCL-2, PI3K, and NRF2. Co-treatment, particularly at 30 mg/kg, was associated with improved sperm motility and concentration, a lower dead sperm rate, reduced histopathological damage, lower NF-κB and caspase-3 abundance, and improvement in selected junctional-protein staining relative to FNS alone. However, abnormal sperm morphology and DNA damage at 30 mg/kg were not significantly different from the FNS group, and PI3K and NRF2 were not significantly restored. Serum testosterone did not differ among groups, whereas OSI showed an overall group effect (p = 0.007). Tissue-specific oxidative stress markers and pathway phosphorylation were not assessed. These findings provide preliminary, associative evidence that ZnO NPs may partially attenuate FNS-associated testicular injury; they do not establish NF-κB/STAT3 signaling or oxidative stress as causal mechanisms.