Therapeutic Effects of Edar avone on Azoospermia: Free Radical Scavenging and Autophagy Modulation in Testicular Tissue of Mice

Background: chemotherapeutic agents such as cyclophosphamide and busulfan have been shown to have a negative impact on the spermatogenesis process. based on this fact, the objective of this study was to investigate the effects of edaravone on spermatogenesis in busulfan-induced mice. methods: forty adult male mice were equally divided into the four groups: 1) control, 2) edaravone, 3) busulfan, and 4) busulfan + edaravone. then, the sperm parameters, histopathological examinations, and serum levels of testosterone, follicle-stimulating hormone (fsh), and luteinizing hormone (lh) were also assessed. caspase-3, beclin-1, and atg-7 mrna levels were also determined using real-time pcr. results: our results revealed that treatment of mice with edaravone in busulfan-induced azoospermia significantly improves sperm parameters, including total count, morphology, and viability (p<0.05). furthermore, edaravone administration led to a significant increase in serum testosterone (p<0.0001) and fsh (p<0.001) levels, as well as testis weight (p<0.05) and volume (p<0.01). edaravone also prevented a decrease in the number of testicular cells including spermatogonia (p<0.0001), primary spermatocytes (p< 0.001), round spermatids (p<0.0001), sertoli (p<0.01), and leydig cells (p<0.0001) in busulfan-treated mice. additionally, in busulfan-induced azoospermia, edaravone significantly reduced the percentage of sperm with immature chromatin (p<0.0001). following treatment with edaravone, a decrease in reactive oxygen species (ros) and an increase in glutathione (gsh) production were noted compared to busulfan-treated mice. furthermore, caspase-3 (p<0.05), beclin-1, and atg-7 (p<0.001) genes expression decreased significantly in treatment groups compared to busulfan-induced azoospermia. conclusion: according to our findings, edaravone can improve spermatogenesis in busulfan-induced azoospermia through free radical scavenging and autophagy modulation in testicular tissue.