CYCLOOXYGENASE-2 APPEARS TO BE INDUCED IN THE TESTES OF EXPERIMENTAL CRYPTORCHIDISM IN ORDER TO REDUCE THE APOPTOSIS OF GERM CELLS AND MAY HAVE A KEY ROLE ON PROTECTION OF GERM CELLS FROM HEAT-STRESS

Abstract

INTRODUCTION AND OBJECTIVES: The roles of Cyclooxygenases (COXs) in the male reproductive tract remain unclear. However, there are some reports that suggest the COX-2 might have effect on spermatogenesis or steroidogenesis. In this study, we examined whether COX-2 is induced in impaired testes and also investigated the possible role of COXs in the testes using experimental cryptorchidism model mice. METHODS: Five-week-old male mice underwent an operation to induce unilateral cryptorchidism by an abdominal incision and suturing of the left testes to the lateral abdominal wall, and were then divided into three groups: (1) experimental cryptorchidism plus SC560 (selective COX-1 inhibitor) administration; (2) experimental cryptorchidism plus NS398 (selective COX-2 inhibitor) administration; (3) experimental cryptorchidism alone. The expressions of COX-1 and COX-2 were determined by immunohistological staining and quantitative reverse transcriptional polymerase chain reaction (RT-PCR). The influence of COX inhibitors on the testis was assessed by measuring the concentration of serum testosterone and evaluating the seminiferous tubules according to the Johnsen score (JS). TdT-mediated dUTP-biotin nick end-labeling (TUNEL) staining was also performed to detect apoptosis in the testes. RESULTS: Immunohistological staining and RT-PCR revealed that the expression of COX-2 was increased in the experimental cryptorchidism testes (group 1-3). The concentration of serum testosterone was significantly lower in group 2 at 5 weeks after surgery than that in other groups; however, not in the level of castration. The Johnsen score of cryptorchidism testes in group 2 was significantly lower than that in other groups at 5 weeks after surgery. TUNEL staining revealed that the apoptotic cells were significantly increased in group 2 compared with that in other groups. Meanwhile, COX-1 inhibitor did not appear to affect spermatogenesis in the experimental cryptorchid testes. CONCLUSIONS: These results suggest that COX-2 inhibitor could reinforce testicular damage in the experimental cryptorchidism by inducing germ cell apoptosis. The expression of COX-2 might be induced to protect germ cells from heat stress caused by experimental cryptorchidism.