Abstract
SummaryVaricocele, defined by a dilation of efferent testicular veins, is the most commonly identifiable, surgically correctable lesion associated with male-factor infertility, starts at puberty and causes a progressive decline in fertility potential. The pathophysiology of infertility caused by this disease is still poorly understood, but it is suggested that the main mechanism is oxidative stress. Therefore, the aim of this study was to verify if the varicocele is associated with changes in enzymatic antioxidant mechanisms and seminal plasma lipid peroxidation levels in adolescents. We recruited 90 adolescents that were divided into control (C; n = 27); varicocele and normal semen (VNS; n =46); varicocele and altered semen (VAS; n =17). Seminal and serum levels of lipid peroxidation were quantified by thiobarbituric acid reactive substances (TBARS). Seminal plasma antioxidant profile was evaluated by the activities of catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD). The VAS group had increased lipid peroxidation levels when compared to the other groups. The levels of serum lipid peroxidation and activities of the enzymes SOD and GPx did not differ between groups. CAT was undetectable by the method used. In conclusion, in adolescents with varicocele and altered semen analysis, there is an increase in seminal lipid peroxidation levels compared to adolescents with varicocele and without seminal change and adolescents without evident varicocele. However, the observed oxidative stress is not caused by a decrease in superoxide dismutase and glutathione peroxidase activities, which did not differ between adolescents with and without evident varicocele.Lay summaryVaricocele, defined by a dilation of efferent testicular veins, is the most commonly identifiable, surgically correctable lesion associated with male-factor infertility, starts at puberty and causes a progressive decline in fertile potential. There is still much that is not understood regarding how exactly it affects semen quality, but most studies agree that oxidative stress, which is defined as excessive amounts of free radicals in relation to antioxidant defense, is an important mechanism. In this study, we aimed to verify if the varicocele is associated with changes in antioxidant defense and semen oxidation in 90 adolescents with and without varicocele. In adolescents with varicocele and abnormal semen, there is an increase in semen oxidation compared to controls or to the group with varicocele and normal semen quality. Our results can help to understand how varicocele leads to infertility in adolescents, identifying changes in oxidative activity in semen, since the onset of varicocele and before damage to sperm production can be detected.
Highlights
Infertility, defined as the couple's failure to conceive after 12 months of regular and unprotected sexual intercourse, affects about 15% of couples in reproductive age and the male factor is associated in up to 50% of cases (Brugh & Lipshultz 2004)
Varicocele was diagnosed by scrotal palpation, with the adolescent in the standing position and in a controlled temperature environment (23–25°C), according to the American Society for Reproductive Medicine (ASRM) guidelines (Practice Committee of the American Society for Reproductive Medicine and Society for Male Reproduction and Urology 2014)
Groups were formed as 27 adolescents in control, 46 in varicocele normal semen and 17 varicocele altered semen
Summary
Infertility, defined as the couple's failure to conceive after 12 months of regular and unprotected sexual intercourse, affects about 15% of couples in reproductive age and the male factor is associated in up to 50% of cases (Brugh & Lipshultz 2004). Its prevalence increases gradually until the age of 15, when it reaches the same prevalence observed in adults: approximately 15% of the male population (Gorelick & Goldstein 1993, Witt & Lipshultz 1993). In order to explain the impaired spermatogenesis commonly observed in these patients, some complementary and interconnected hypotheses have been postulated: (i) an increase in scrotal and testicular temperature; (ii) presence of testicular hypoxia; (iii) presence of reflux in kidney and adrenal metabolites; (iv) decreased perfusion of the affected testicle caused by increased venous pressure; and (v) hormonal dysfunction (Jensen et al 2017)
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