Oxidative status in testis and epididymal sperm parameters after acute and chronic stress by cold-water immersion in the adult rat

Abstract

Stress is associated with detrimental effects on male reproductive function. It is known that stress increases reactive oxygen species (ROS) generation in the male reproductive tract. High ROS levels may be linked to low sperm quality and male infertility. However, it is still not clear if ROS are generated by stress in the testis. The objective of this study was to characterize the role of oxidative stress induced by cold-water immersion stress in the testis of adult male rats and its relation with alterations in cauda epididymal sperm. Adult male rats were exposed to acute stress or chronic stress by cold-water immersion. Rats were sacrificed at 0, 6, 12, and 24 hours immediately following acute stress exposure, and after 20, 40, and 50 days of chronic stress. ROS production increased only at 6 hours post-stress, while the activity and expression of antioxidant enzymes, lipid peroxidation (LPO), and sperm parameters were not modified in the testis. Corticosterone increased immediately after acute stress, whereas testosterone was not modified. After chronic stress, testicular absolute weight decreased; in addition, ROS production and LPO increased at 20, 40, and 50 days. The activity of superoxide dismutase (SOD) and glutathione peroxidase (GPx) decreased throughout the duration of chronic stress and the activity of catalase (CAT) decreased at 40 and 50 days, and increased at 20 days. The expression of copper/zinc superoxide dismutase (SOD1) and CAT were not modified, but the expression of phospholipid hydroperoxide glutathione peroxidase (GPx-4) decreased at 20 days. Motility, viability, and sperm count decreased, while abnormal sperm increased with chronic stress. These results suggest that during acute stress there is a redox state regulation in the testis since no deleterious effect was observed. In contrast, equilibrium redox is lost during chronic stress, with low enzyme activity but without modifying their expression. In addition, corticosterone increased while testosterone decreased, this decrease is related to the negative effects seen in sperm.

Cold stress increases reactive oxygen species formation via TRPA1 activation in A549 cells

“…It has been reported that cold stress increased the production of ROS in animal model and cellular and mitochondrial experiments, respectively (Ali et al 2010;García-Díaz et al 2015;Awad et al 2013). Our results suggest that TRPA1 is mainly involved in the production of ROS via [Ca 2+ ] c elevation pathway induced by cold stress in lung epithelial cell.…”

Effect of folate deficiency on promoter methylation and gene expression ofEsr1, Cav1, andElavl1, and its influence on spermatogenesis

“…Epididymal sperm count was determined as previously described [46]. Epididymis was collected from each group at the end of the 8th week and homogenized in 1 mL of saline.…”

Stress and Cell Death in Testicular Cells

“…It has been proposed that the activation of apoptosis in these cells may be related to the activation of the Fas system of procaspase 3 with the loss of mitochondrial membrane potential and the increase in the generation of ROS [3]. As mentioned above, the increase in glucocorticoid concentration may be related to the activation of apoptosis in testicular cells through an increase in ROS generation [48]. Oxidative stress may be related to various etiologies that cause infertility in various species of male mammals, including humans [64].…”

“…Cold water immersion stress (15°C for 15 min) applied to rats for 1, 20, 40 and 50 consecutive days has been shown to increase the percentage of seminiferous tubules containing apoptotic germ cells positive for TUNEL (Terminal deoxynucleotidetransferase). In addition, this stressor increases the generation of reactive oxygen species (ROS), such as hydrogen peroxide (H 2 O 2 ), and peroxidation of (H 2 O 2 ) (SOD), catalase (CAT), and glutathione peroxidase (Gpx) [48]. In the testes, H 2 O 2 has the ability to induce apoptosis in testicular cells involving the Fas system and its ligand (FasL) as well as pro-apoptotic proteins: Bax, Bid and Bad [36].…”