Received January 14, 2026
Accepted February 09, 2026

Background: Testicular torsion (TT) causes necrosis, while sudden blood flow restoration to prevent testicular death results in testicular ischemia-reperfusion injury (TIRI). This leads to testicular damage and potentially long-term infertility. All-trans retinoic acid (ATRA) has been shown to improve the transcription of antioxidant enzymes and anti-apoptotic proteins, inhibit NF-κB-mediated transcription of inflammatory cytokines, and support the differentiation of germ cells and spermatogenesis. Aim: This study investigated the protective role of ATRA on the ipsilateral testes following unilateral testicular torsion/detorsion. Materials and Methods: Twenty-four male Wistar rats were divided into four groups (n=6): Sham, Torsion/Detorsion (TD), ATRA + TD (7.5 mg/kg administered 3 days before TIRI induction), and TD + ATRA (7.5 mg/kg administered 3 days after TIRI induction). Torsion was induced for 1 hour; detorsion followed immediately. Results: TD resulted in reduced levels of reproductive hormones (testosterone, inhibin), Bcl-2, sperm indices, SOD, CAT, GPx, GST, GSH, and total protein, with concomitant increase in testicular MDA, NO, TNF-α, MPO, 1L-6, NF-κB, Bax, caspase-3, TDFI and 8-OHdG levels. Histological evaluation of TD rats revealed reduced spermatogenesis indices, disruption of the seminiferous tubules, loss of germ cells, and vascular congestion. ATRA treatment significantly improved antioxidant enzymes, down-regulated NF-κB and Bax signalling, restored reproductive hormones, sperm parameters, and conferred protection on testicular and epididymal structures. Conclusion: ATRA protects against ipsilateral testicular damage following torsion/detorsion, evidenced by the restoration of depleted antioxidant enzymes, downregulation of inflammatory and pro-apoptotic markers, and enhancement of spermatogenesis and hormonal balance. These findings support ATRA’s potential role in preserving fertility after testicular torsion/detorsion.