Protective action of N-acetylcysteine on sperm quality in cyclophosphamide-induced testicular toxicity in male Wistar rats

BACKGROUND: Reductions in sperm quality due to free radical formation during cancer chemotherapy are well documented, hence the need for an adjunct antioxidant treatment during chemotherapy. This study was designed to investigate the effects of N-acetylcysteine on sperm quality following cyclophosphamide exposure in male Wistar rats. METHODS: Twenty male Wistar rats weighing 150-170g were randomly assigned into 4 groups of five rats each, and were orally administered distilled water (Control), Cyclophosphamide (6mg/kg), N-acetylcysteine (100mg/kg) or Cyclophosphamide + N-acetylcysteine for 21 days. Sperm count, histone-protamine replacement, chromatin integrity, testicular histomorphometry and BAX Protein expression were assessed using standard procedures. The data was presented as mean ± SEM and analyzed using students' t- test. A p<0.05 was considered significant. RESULTS: Sperm counts were significantly reduced (p<0.05) among the cyclophosphamide (69.95±7.78 x10(6)/ml) and cyclophosphamide + N-acetylcysteine (64.78±3.52 x10(6)/ml) treated rats, while it increased significantly (p<0.05) in the N-acetylcysteine (132.20±28.71 x10(6)/ml) treated rats compared to the control animals (115.30±8.70x10(6)/ml). Increased interstitial space distance, degenerated Leydig cells and impaired histone-protamine replacement observed among the cyclophosphamide-treated rats were ameliorated in the cyclophosphamide + N-acetylcysteine-treated rats. Sperm chromatin integrity, which was poor in the cyclophosphamide-treated rats, was considerably improved when compared with the Control and the N-acetylcysteine-treated rats. Bax protein expression was reduced in the cyclophosphamide (20%) and cyclophosphamide+N-acetylcysteine (20%) groups when compared with the Control (50%) and N-acetylcysteine (50%) groups. CONCLUSION: We concluded that N-acetylcysteine might improve sperm histone protamine replacement, which is one of the stage-specific effect of cyclophosphamide toxicity.