Whole-body heat exposure induces membrane changes in spermatozoa from the cauda epididymidis of laboratory mice
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Updated: Jun 12, 2026

A Preclinical Model of Exertional Heat Stroke in Mice
Published on: July 1, 2021
Harsha Wechalekar1, Brian P Setchell, Eleanor J Peirce
1Discipline of Anatomy and Pathology, School of Medical Sciences, Faculty of Health Sciences, University of Adelaide, Adelaide, South Australia, Australia.
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 37 degrees C-38 degrees C for 8 h per day for three consecutive days, while control mice (n = 7) were kept at 23 degrees C-24 degrees C. 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 37 degrees C-38 degrees C induces membrane changes in the epididymal spermatozoa of mice, which may lead to apoptosis.
Insights
Exposure to hot environmental temperatures significantly reduced sperm motility and induced membrane changes in mice. Heat stress impacts sperm quality, potentially leading to apoptosis and affecting male fertility.
Area of Science:
- Reproductive Biology
- Environmental Health
- Spermatozoa Physiology
Background:
- Elevated environmental temperatures are a potential stressor for male reproductive health.
- Understanding the impact of heat exposure on sperm quality is crucial for reproductive medicine.
Purpose of the Study:
- To investigate the detrimental effects of whole-body heat exposure on epididymal sperm quality in mice.
- To assess the impact of controlled high temperatures on sperm motility and membrane integrity.
Main Methods:
- C57BL/6 mice were exposed to high temperatures (37°C–38°C) for 8 hours daily over three days.
- Control mice were maintained at standard room temperature (23°C–24°C).
- Sperm motility and membrane integrity (using Annexin V-PE and 7-AAD staining) were assessed post-exposure.
Main Results:
- Sperm numbers remained comparable between heat-exposed and control groups.
- A significant reduction in sperm motility was observed in heat-exposed mice (P < 0.0001).
- Heat exposure led to a significant increase in spermatozoa with altered membrane integrity (P < 0.05).
Conclusions:
- Whole-body heat exposure at 37°C–38°C negatively impacts mouse sperm motility and induces plasma membrane damage.
- These heat-induced changes in spermatozoa may contribute to apoptosis and reduced male fertility.
- Environmental heat stress poses a risk to sperm quality and reproductive potential.
