Abstract
Higher temperatures lead to an increase of testicular metabolism that results in spermatic damage. Oxidative stress is the main factor responsible for testicular damage caused by heat stress. The aim of this study was to evaluate lasting effects of heat stress on ejaculated sperm and immediate or long-term effects of heat stress on epididymal sperm. We observed decrease in motility and mass motility of ejaculated sperm, as well as an increase in the percentages of sperm showing major and minor defects, damaged plasma and acrosome membranes, and a decrease in the percentage of sperm with high mitochondrial membrane potential in the treated group until one spermatic cycle. An increased enzymatic activity of glutathione peroxidase and an increase of stressed cells were observed in ejaculated sperm of the treated group. A decrease in the percentage of epididymal sperm with high mitochondrial membrane potential was observed in the treated group. However, when comparing immediate and long-term effects, we observed an increase in the percentage of sperm with low mitochondrial membrane potential. In conclusion, testicular heat stress induced oxidative stress that led to rescuable alterations after one spermatic cycle in ejaculated sperm and also after 30 days in epididymal sperm.
Highlights
The testicle is the organ of the male reproductive tract responsible for spermatogenesis
No differences were observed between groups and between immediate and long-term effects of heat stress on epididymal sperm in any categories of plasma and acrosome membranes integrity
No differences were observed between groups and between immediate and long-term effects of heat stress considering glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity in epididymal sperm
Summary
The testicle is the organ of the male reproductive tract responsible for spermatogenesis. Similar to organ transplantation procedures, a phenomenon known as hypoxia-reperfusion injury may occur [3, 4] In this condition, the oxidative imbalance may occur after the reestablishment of the normal temperature and tissue reperfusion. The oxidative imbalance may occur after the reestablishment of the normal temperature and tissue reperfusion This situation has been described in studies where suppression of testicular function under heat stress led to a decrease in fertility in ruminants [5, 6], murine [7], and human affected by varicocele [8]. These studies concluded that oxidative stress is the main factor responsible for damage caused by heat stress
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
