Ketoprofen and meloxicam impair spermatogenesis and alter testicular histomorphology in rats
TL;DR
Findings indicate that subacute NSAID exposure compromises seminiferous epithelium architecture and spermatogenesis in rats, with ketoprofen inducing more pronounced deleterious effects on male reproductive function.
Abstract
Abstract This study evaluated the effects of the nonsteroidal anti-inflammatory drugs (NSAIDs) ketoprofen and meloxicam on testicular morphology and spermatogenic dynamics in rats. Adult Wistar rats were treated by oral gavage once daily for 15 days with meloxicam (1 mg/kg) or ketoprofen (5 mg/kg). No significant differences were observed among groups regarding testicular biometric and volumetric parameters. However, both treatments significantly reduced Sertoli cell numbers (8.1% in ketoprofen and 9.2% in meloxicam group). Ketoprofen induced more pronounced reductions in type A spermatogonia (35.1%), primary spermatocytes (36.9%), and round spermatids (42.2%) number, whereas meloxicam caused milder decreases (12.2%, 12.2% and 14.3%, respectively). Only ketoprofen significantly impaired spermatogenic dynamics, reducing mitotic, meiotic, and spermatogenic yields, as well as Sertoli cell efficiency. Histometric analysis revealed a marked increase in tubular lumen area (54% in ketoprofen and 113% in meloxicam groups) and a reduction in seminiferous epithelium height (25% and 43%, respectively) in treated groups. In addition, cytoplasmic vacuolization in Sertoli cells was observed in both treated groups. These findings indicate that subacute NSAID exposure compromises seminiferous epithelium architecture and spermatogenesis in rats, with ketoprofen inducing more pronounced deleterious effects on male reproductive function.