Abstract
Oxidative stress is a common culprit of several conditions associated with male fertility. High levels of reactive oxygen species (ROS) promote impairment of sperm quality mainly by decreasing motility and increasing the levels of DNA oxidation. Oxidative stress is a common feature of environmental pollutants, chemotherapy and other chemicals, smoke, toxins, radiation, and diseases that can have negative effects on fertility. Peroxiredoxins (PRDXs) are antioxidant enzymes associated with the protection of mammalian spermatozoa against oxidative stress and the regulation of sperm viability and capacitation. In the present study, we aimed to determine the long-term effects of oxidative stress in the testis, epididymis and spermatozoa using the rat model. Adult male rats were treated with tert-butyl hydroperoxide (t-BHP) or saline (control group), and reproductive organs and spermatozoa were collected at 3, 6, and 9 weeks after the end of treatment. We determined sperm DNA oxidation and motility, and levels of lipid peroxidation and protein expression of antioxidant enzymes in epididymis and testis. We observed that cauda epididymal spermatozoa displayed low motility and high DNA oxidation levels at all times. Lipid peroxidation was higher in caput and cauda epididymis of treated rats at 3 and 6 weeks but was similar to control levels at 9 weeks. PRDX6 was upregulated in the epididymis due to t-BHP; PRDX1 and catalase, although not significant, followed similar trend of increase. Testis of treated rats did not show signs of oxidative stress nor upregulation of antioxidant enzymes. We concluded that t-BHP-dependent oxidative stress promoted long-term changes in the epididymis and maturing spermatozoa that result in the impairment of sperm quality.
Highlights
Infertility is a concerning pathophysiological condition that affects about 16% of couples worldwide, and approximately half of the cases are attributable to male factors [1]
We previously reported that spermatozoa from rats challenged with an in vivo oxidative stress using tert-butyl hydroperoxide (t-BHP), and collected 24 h after the treatment, have higher levels of DNA oxidation and lipid peroxidation and displayed poor motility compared to untreated controls [18]
Spermatozoa from t-BHP-treated animals showed a significant reduction of their motility at all times compared to those sperm from the control group
Summary
Infertility is a concerning pathophysiological condition that affects about 16% of couples worldwide, and approximately half of the cases are attributable to male factors [1]. Even though the cause for the majority of the male infertile cases is unknown, oxidative stress caused by a high amount of reactive oxygen species (ROS) has been observed in 30–80% of infertile patients [2,3]. Even though low ROS levels are required for the acquisition of fertilization ability by the spermatozoon [9], oxidative stress damages spermatozoa by reducing motility, and increasing levels of DNA, protein oxidation and lipid peroxidation [10,11,12]. As occurring in somatic cells, this oxidative stress observed in spermatozoa is the result of an imbalance between the antioxidant defense system and the endogenous generation of ROS.
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