The role of sST2 and galectin-3 in testicular torsion ischemia reperfusion injury: Rat study

Introduction: Testicular torsion is an urological emergency that occurs due to twisting of the spermatic cord, resulting in interruption of blood flow to the testis. Diagnosis is established based on history, physical examination, and scrotal color doppler ultrasonography findings. However, despite these evaluations, some cases remain diagnostically uncertain. The aim of this study was to identify a specific biomarker associated with ischemia-reperfusion injury caused by testicular torsion. Material and methods: Fifty male wistar albino rats were randomly divided into five groups: control, sham, early torsion, torsion, and torsion-detorsion. Blood samples were collected from the control group without surgical intervention. In the sham group, blood was obtained following scrotal exploration. In the early torsion group, blood samples were collected after 15 minutes of torsion. In the torsion group, samples were taken after 2 hours of torsion, while in the torsion-detorsion group, samples were collected following 2 hours of torsion and 2 hours of detorsion. The left testes of all rats were excised after blood collection. Serum galectin-3 and soluble suppression of tumorigenicity 2 (sST2) levels were measured using the enzyme-linked immunosorbent assay (ELISA) method. Histopathological damage in testicular tissues was evaluated using seminiferous tubule diameter, germinal epithelial thickness, and johnsen testicular biopsy score (JTBS) to assess spermatogenesis. Results: No statistically significant difference was observed among the groups in terms of galectin-3 levels. However, compared to the control group, sST2 levels were significantly increased in the early torsion, torsion, and torsion-detorsion groups. Seminiferous tubule diameter, JTBS, and germinal epithelial thickness were significantly decreased in the torsion and torsion-detorsion groups compared to the control group, whereas no significant differences were found in the sham and early torsion groups. A significant negative correlation was determined between sST2 levels and both seminiferous tubule diameter and JTBS. Conclusion: This study demonstrated that sST2 may be a potential biomarker for the early diagnosis of ischemia-reperfusion injury secondary to testicular torsion. However, galectin-3 levels did not show a significant difference among the groups, possibly due to its delayed release in testicular tissue or its limited systemic circulation. Further large-scale and advanced studies are required to clarify this finding. In addition, this study is significant as it is the first to investigate the relationship between sST2 and galectin-3 levels in testicular torsion. Key Words: Testicular torsion; Ischemia-reperfusion; sST2; Galectin-3; Biomarker