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  • Title: Immunohistopathology of the contralateral testis of rats undergoing experimental torsion of the spermatic cord.
    Author: Rodriguez MG, Rival C, Theas MS, Lustig L.
    Journal: Asian J Androl; 2006 Sep; 8(5):576-83. PubMed ID: 16847529.
    Abstract:
    AIM: To evaluate the immunohistopathological changes in the contralateral testis of rats after an experimental spermatic cord torsion. METHODS: Male Sprague-Dawley rats of 45-50 days old were subjected to a 720 degree unilateral spermatic cord torsion for 10, 30 and 80 days (experimental group, E), respectively or sham operation (control group, C). Histopathology of the contralateral testis as well as germ cell apoptosis were studied using the Terminal Deoxynucleotidyl Transferase Biotin-dUTP Nick End Labeling (TUNEL) technique. The number of testicular lymphocytes, mast cells and macrophages, and the expression of tumor necrosis factor-alpha (TNF-alpha) and its receptor (TNFR1) in testicular cells of the contralateral testis were quantified by histochemistry and immunohistochemistry. TNF-alpha concentration in testicular fluid was determined by ELISA. RESULTS: In the contralateral testis of rats from the E group, the maximal degree of damage of the germinal epithelium was seen 30 days after torsion. At this time we observed in the E group vs. the C group increases: (i) the number of testicular T-lymphocytes; (ii) the number of testicular mast cells and macrophages; (iii) the percentage of macrophages expressing TNF-alpha; (iv) TNF-a concentration in testicular fluid; (v) the number of apoptotic germ cells; and (vi) the number of TNFR1+ germ cells. CONCLUSION: Experimental spermatic cord torsion induces, in the contralateral testis, a focal damage of seminiferous tubules characterized by apoptosis and sloughing of germ cells. Results suggest humoral and cellular immune mediated testicular cell damage in which macrophages and mast cells seem to be involved in the induction of germ cell apoptosis through the TNF-alpha/TNFR1 system and in the modulation of the inflammatory process.
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