The evaluation of the reproducti?ve toxicity of naproxen sodium and meloxicam in male rats

Nonsteroidal anti-inflammatory drugs which are cyclooxygenase (COX) enzyme inhibitors have generally been used in short-term pain management and also to treat inflammation chronically. It is known that COX enzyme and prostaglandins had important roles in the regulation of reproductive functions in females. However, there are relatively few studies for male reproductive system and results of these studies are contradictory. In this study, sperm parameters like sperm count and motility, COX-1, COX-2 enzyme activities, prostaglandin E1 (PGE1), prostaglandin E2 (PGE2) and prostaglandin F2? (PGF2?) levels in testis tissue, plasma FSH, LH and testosterone levels and histopathological examination of testis tissue were evaluated after naproxen sodium and meloxicam administration in male rats. Also, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione (GSH) levels were measured to investigate the oxidative status induced secondarily to the inhibition of prostaglandin synthesis. According to our results, sperm count and motility were significantly were decreased in treatment groups compared to control group. In testis tissue, COX-1, PGE2 and PGF2? levels were significantly decreased after naproxen sodium and meloxicam administration, while the decreases of COX-2 and PGE1 levels did not show significance statistically. In treatment groups, plasma FSH, LH and testosterone levels did not show any significant difference compared to control group. Testis SOD, catalase, GPx and GSH levels were decreased significantly after naproxen sodium and meloxicam administration. According to the results of histopathological examination, damage in seminiferous tubules, where spermatogenesis developed, was observed. In conclusion, it was showed that prostaglandin inhibition decreased sperm count and motility and also induced the damage of seminiferous tubules as a direct effect without affecting plasma hormone levels in our study.Furthermore, oxidative stress is induced as a secondary factor by these agents.