Mitochondrial transplantation attenuates apoptosis and improves spermatogenic function following testicular torsion-detorsion injury in rats.
7 affiliations
- 1Department of Urology, Gülhane Training and Research Hospital, Ankara-Türkiye.
- 2Department of Urology, Etlik City Hospital, Ankara-Türkiye.
- 3Department of Pharmacology, Ankara University Faculty of Pharmacy, Ankara-Türkiye.
- 4Department of Mitochondria and Cellular Research, Gülhane Health Sciences Institute, University of Health Sciences, Ankara-Türkiye.
- 5Department of Pathology, Gülhane Training and Research Hospital, University of Health Sciences, Ankara-Türkiye.
- 6Department of Urology, Bilkent City Hospital, Ankara-Türkiye.
- 7Institute of Transplantation and Gene Sciences, Başkent University, Ankara-Türkiye.
Abstract
Background
Testicular 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.Methods
Thirty-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.Results
The 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.Conclusion
Intratesticular 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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BibTeX
@article{ozcan2026mitochondrial,
title = {{Mitochondrial transplantation attenuates apoptosis and improves spermatogenic function following testicular torsion-detorsion injury in rats.}},
author = {Cihat Ozcan and Adem Sancı and Umur Deniz Mendeş and Merve Sözer and Öner Ülger and Gülçin Şimşek and Muhammed Mustafa Ayturk and Alper Murat Albayrak and Serap Gür and Cevdet Serkan Gökkaya and Gökhan Burçin Kubat},
journal = {Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma \& emergency surgery : TJTES},
year = {2026},
month = oct,
doi = {10.14744/tjtes.2026.02503},
url = {https://europepmc.org/article/MED/42841884},
note = {CC BY-NC},
}
RIS
TY - JOUR
TI - Mitochondrial transplantation attenuates apoptosis and improves spermatogenic function following testicular torsion-detorsion injury in rats.
AU - Cihat Ozcan
AU - Adem Sancı
AU - Umur Deniz Mendeş
AU - Merve Sözer
AU - Öner Ülger
AU - Gülçin Şimşek
AU - Muhammed Mustafa Ayturk
AU - Alper Murat Albayrak
AU - Serap Gür
AU - Cevdet Serkan Gökkaya
AU - Gökhan Burçin Kubat
PY - 2026
DA - 2026/10/01
JO - Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES
DO - 10.14744/tjtes.2026.02503
UR - https://europepmc.org/article/MED/42841884
AB - Background Testicular 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.Methods Thirty-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.Results The 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.Conclusion Intratesticular 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.
SN - 1306-696X
SN - 1307-7945
ER -