ArticleUlusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES2026
Mitochondrial transplantation attenuates apoptosis and improves spermatogenic function following testicular torsion-detorsion injury in rats.
Article in Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundTesticular torsion is a urological emergency that may result in irreversible ischemia-reperfusion injury and longterm impairment of spermatogenic function despite timely surgical detorsion. Mitochondrial dysfunction plays a central role in oxidative stress-induced germ cell damage following torsion. This study aimed to investigate the protective effects of isolated intratesticular mitochondrial transplantation in a rat model of testicular torsion-detorsion injury.
methodsThirty-six adult male Sprague-Dawley rats were randomly allocated into four groups: sham (n=4), torsion (n=10), torsion+vehicle (n=10), and torsion+mitochondria (n=10). Testicular torsion was induced by a 720° rotation for 2 h, followed by surgical detorsion. Isolated mitochondria were administered through intratesticular injection before torsion induction. Histopathological evaluation was performed using hematoxylin-eosin staining and quantified by the Johnsen scoring system. Apoptotic activity was assessed by Caspase-3 immunohistochemistry. Functional outcomes were evaluated through total sperm count, motile sperm count, and detailed sperm motility subtype analysis.
resultsThe torsion and vehicle groups demonstrated marked histological damage, significantly reduced Johnsen scores, and increased apoptotic activity compared with the sham group. Mitochondrial transplantation significantly preserved seminiferous tubular architecture and resulted in higher Johnsen scores compared with untreated torsion (9.7±0.4 vs. 6.4±1.0, p<0.001). Caspase-3 expression was significantly reduced in the mitochondria-treated group, approaching levels observed in sham animals. Functionally, total and motile sperm counts were significantly higher in mitochondria-treated rats than in torsion and vehicle groups. Detailed motility analysis revealed restoration of progressive sperm motility patterns, whereas progressive motility was completely absent in untreated ischemic groups.
conclusionIntratesticular mitochondrial transplantation provides significant structural and functional protection against ischemia-reperfusion injury in experimental testicular torsion. By preserving spermatogenic architecture, reducing apoptosis, and restoring progressive sperm motility, mitochondrial therapy represents a promising experimental strategy for fertility preservation in ischemic testicular disorders.
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