P-87: Effect of Oxidative Stress on Sperm quality and Testis Histopathology in Mature Male Mice

Background: Infertility is a major clinical and worldwide reproductive problem that affects approximately 15% of young couples. The male factors are responsible for periphery 50 percent of these cases. Recently, the generation of oxidative stress, also described as an imbalance between the production of Reactive oxygen species (ROS) and the body’s antioxidant defence mechanisms, in the male reproductive tract has become a real concern. This is result of their potential toxic effects, at high levels, on sperm quality and function. ROS, defined as including oxygen ions, free radicals and peroxides are generated by sperm and seminal leukocytes within semen and produce infertility by two key mechanisms. First, they damage the sperm membrane, decreasing sperm motility and its ability to fuse with the oocyte. Second, ROS can alter the sperm DNA, resulting in the passage of defective paternal DNA on to the conceptus. Therefore It seems to be a powerful mechanism that can lead to sperm damage, deformity and eventually, male infertility. Materials and Methods: In our study, we used mature male BALB/c mice treated by tertiary-butyl hydroperoxide (TBHP) for 2 weeks by intraperitoneally injection (1/10 LD50 = 7/06µl per 100 g body weight), in order to study of oxidative stress. After that, testis tissue utilized for cell viability, pathology analysis and ROS assay by flowcytometry. Also Epididymis was surveyed for sperm analysis. Results: In the TBHP treated animals, Sperm motility, count and vitality also H2O2 level were significantly reduced. Testis pathology assay demonstrated that some tissues after treatment were without spermatozoid and germ cells stopped in spermiogenesis. Conclusion: The present study designed to investigate the effect of oxidative stress on sperm quality, vitality and testis pathology in male mice exposed to TBHP in comparison to control samples. Previous studies, demonstrated that TBHP inhibits mitochondrial respiratory-chain enzymes such as SOD. This enzyme catalyzed O2.- conversion reaction to H2O2. These results are explanatory of oxidative stress induction. Consequently, this phenomenon leads to decrease of sperm vitality and motility, cells viability and H2O2 level in testis. Also blocking of germ cells in spermiogenesis phase and lake of spermatozoid in some treated testises or decreases of spermatozoids in the other tissues are additional outcomes of this process.