We investigated role of
reactive oxygen species (ROS) and apoptosis in the pathogenesis of
infertility in experimental model of
varicocele. The protective effect of
vitamin E was also examined. Three groups of rats were constructed as the first group had
sham operation, experimental
varicoceles were established by partial
ligation of the left renal vein in later two groups. Third group had received
vitamin E. Production of ROS was determined by chemiluminescence assay (CL). The in situ end labelling technique was utilized to investigate apoptosis. Tissue
vitamin E levels were measured by high performance liquid chromatography. The differences between
luminol enhanced CL levels of groups were not statistically significant. However, the difference between CL levels of
lucigenin probe in left testicles of
sham and
varicocele groups were statistically significant ( p = 0.0007). Similarly, the results of the third group receiving
vitamin E significantly differed from the
varicocele group ( p = 0.0025). The difference of apoptotic index was also statistically significant between
sham and
varicocele groups ( p = 0.0038). Although the values of apoptotic index detected in the
vitamin E group were lower compared with the
varicocele group, the difference was not significant. This study proposes that ROS production and apoptosis in the testicles were induced with experimental
varicocele.
Vitamin E had a protective role. An increased rate of apoptosis with experimental
varicocele suggests a molecular alteration, which may involve ROS overproduction as the triggering mechanism. Consequently, this study indicates an association between
varicocele and
infertility at molecular level through stimulation of ROS and apoptosis.