Heat Stress Effects on Male Germ Cell Viability
Summary
Heat stress poses a significant challenge to male reproductive health by disrupting the finely tuned environment required for spermatogenesis. Elevated testicular temperature can impair the protective functions of Sertoli and Leydig cells, provoke an excess of reactive oxygen species and instigate endoplasmic reticulum stress, all of which culminate in diminished germ cell viability. Such thermal insults undermine DNA integrity, lipid homeostasis and mitochondrial function, triggering autophagy or programmed cell death pathways in spermatogonia, spermatocytes and spermatids. In turn, sperm motility and morphology deteriorate, reducing fertilisation potential. These effects have far-reaching implications, from declining fertility rates in human populations exposed to high ambient temperatures to economic losses in livestock industries. Advances in molecular understanding have highlighted oxidative stress as a central mechanism and spurred development of antioxidant, hormonal and lifestyle interventions aimed at preserving germ cell health under hyperthermic conditions.
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Heat Stress Effects on Male Germ Cell Viability publication trend
The graph below shows the total number of articles in heat stress effects on male germ cell viability across all publications each year (not limited to Nature Index journals).
Technical terms
Reactive oxygen species (ROS): Highly reactive molecules derived from oxygen that can damage lipids, proteins and DNA.
Autophagy: A cellular self-digestion process that recycles damaged organelles and proteins, often activated under stress.
Apoptosis: Programmed cell death characterised by organised cellular breakdown, which eliminates damaged or dysfunctional cells.
Endoplasmic reticulum stress: A state in which unfolded or misfolded proteins accumulate in the endoplasmic reticulum, triggering adaptive or apoptotic pathways.
Sertoli cells: Somatic cells within the seminiferous tubules that nourish and support developing germ cells during spermatogenesis.
References
- Heat stress upregulates arachidonic acid to trigger autophagy in sertoli cells via dysfunctional mitochondrial respiratory chain function. Journal of Translational Medicine (2024).
- Advancements in Genetic Biomarkers and Exogenous Antioxidant Supplementation for Safeguarding Mammalian Cells against Heat-Induced Oxidative Stress and Apoptosis. Antioxidants (2024).
- Melatonin relieves heat-induced spermatocyte apoptosis in mouse testes by inhibition of ATF6 and PERK signaling pathways. 动物学研究 (2021).
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