The role of reactive oxygen species and apoptosis in the pathogenesis of varicocele in a rat model and efficiency of vitamin E treatment

Abstract

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.

Outcome of Varicocelectomy with Different Degrees of Clinical Varicocele in Infertile Male

“…Research conducted during the last decade has provided growing support to the concept that oxidative stress (OS) is one of the main causes of male infertility. Reactive oxygen species may also act through induction of apoptosis [12]. Turkyilman et al implicated that elevated nitric oxide (NO) may be another mechanism of injury in varicoceles, independent of other free radicals [13].…”

Preventive effect of tert-butylhydroquinone on scrotal heat-induced damage in mouse testes

“…Many natural antioxidants can be effectively applied to eliminate oxidative stress by reducing the level of testicular-free radicals, including vitamin E (Cam et al, 2004), vitamin C, L-cysteine, and diphenyl-phenylene-diamine (Ahmed et al, 2011). In this study, we used tBHQ, which is not only a direct antioxidant used to preserve various oils, fats, and food by inhibiting autopolymerization of organic peroxides (de Guzman et al, 2009), but is also an indirect antioxidant acting as a nuclear factor erythroid 2-related factor 2 activator (Nrf2) to promote its accumulation in the nucleus and up-regulating the expression of antioxidant genes against oxidative stress (Cheung et al, 2011;Saykally et al, 2012).…”

Varicocele and Male Infertility: Current Issues in Management-A Review

“…It may also induce spontaneous death of mature sperms. Cam et al [32] and Barqawi et al [33] in their experimental rat model studies of varicocele found an increased rate of apoptosis in varicocele group, when compared to the sham surgery group. This apoptosis may be ROS mediated, and could be reversed through the use of antioxidants (i.e.…”