Whole-body heat exposure induces membrane changes in spermatozoa from the cauda epididymidis of laboratory mice

Abstract

This study was carried out to determine if exposure to hot environmental temperatures had a direct, detrimental effect on sperm quality. For this the effect of whole-body heat exposure on epididymal spermatozoa of laboratory mice was investigated. C57BL/6 mice (n = 7) were housed in a microclimate chamber at 37ºC-38ºC for 8 h per day for three consecutive days, while control mice (n = 7) were kept at 23ºC-24ºC. Cauda epididymal spermatozoa were obtained 16 h after the last heat treatment. The results showed that sperm numbers were similar in the two groups (P = 0.23), but after heat treatment, a significant reduction in the percentage of motile sperm was present (P < 0.0001). Membrane changes of the spermatozoa were investigated by staining with phycoerythrin (PE)-conjugated Annexin V, which detects exteriorization of phosphotidylserine from the inner to the outer leaflet of the sperm plasma membrane, and 7-aminoactinomycin D (7-AAD), which binds to the sperm nucleus when the plasma membrane is damaged. The percentage of spermatozoa showing positive staining with Annexin V-PE or 7-AAD or both, was significantly higher (P < 0.05) in heat-exposed mice compared with controls. These results show that whole-body heat exposure to 37ºC-38ºC induces membrane changes in the epididymal spermatozoa of mice, which may lead to apoptosis.

Royal jelly protects male rats from heat stress‐induced reproductive failure

“…It is clear that psychological and physiological effects of stress can lead to endocrine and functional disorders in the testis (Pook, Tuschen‐Caffier, & Krause, ). Moreover, previous reports have demonstrated that HS exposure induces sperm motility reduction and sperm chromatin abnormality and apoptosis increases (Sailer, Sarkar, Bjordahl, Jost, & Evenson, ; Wechalekar et al, ). Therefore, HS affects reproductive performance and can result in human and animal infertility (Setchell, ; Venkatachalam & Ramanathan, ).…”

“…It has been shown that experimental scrotal hyperthermia leads to suppressing spermatogenesis in several studies in rats (Guo et al, ), mice (Li et al, ), monkeys (Zhang et al, ) and humans (Rao et al, ). Moreover, it is well documented that intratesticular temperature increase has adverse effects on spermatogenesis; thus, extrinsic HS in the scrotum may have been associated with sperm abnormality and spermatozoa apoptosis (Jung & Schuppe, ; Wechalekar et al, ).…”

Impact of quercetin supplementation on testicular functions in summer heat-stressed rabbits

“…Sperm motility can be restored by increasing the level of ATP in sperm suspending media (Gong et al, 2017). Increased environmental (Gong et al, 2017) or body temperature (Wechalekar et al, 2010) affect the mitochondrial activity by inducing oxidative stress (Zhao et al, 2006). Recently, it has been observed that oxidative phosphorylation level, ATP contents and sperm motility events are linked to each other (Guo et al, 2017) and low mitochondrial activity due to HS affect the whole pathway of sperm motility (Gong et al, 2017).…”

An Accidental Andrologist

“…I am currently cosupervisor of three Ph.D. students, one in Anatomical Sciences looking at the effects of heat on epididymal spermatozoa [100] and two in the Department of Obstetrics and Gynecology working on the effects of obesity on reproduction in males [101,102]. I continue to referee papers for a range of journals and try to attend relevant scientific meetings whenever possible.…”