Abstract Spermatogenesis is highly dependent on scrotal temperature. In the testis, germ cells but not somatic cells are vulnerable to heat stress. In response to heat stress, germ cells undergo apoptosis, autophagy, necrosis, and cell cycle arrest; these behaviors are different in each testicular component. Heat induces oxidative stress in the testicles in a variety of ways, mainly by lipid peroxidation of the cellular membrane and mitochondria-derived reactive oxygen species (ROS), and heat-induced oxidative stress is involved in all of these cellular behaviors. Heat-shock factor 1 (HSF1) protects the cells by regulating the expression of heat-shock proteins (HSPs), promoting cell survival. Paradoxically, HSF1 promotes apoptosis of germ cells by heat stress, indicating that injured germ cells actively undergo apoptosis to maintain the quality of gametes. The pattern of heat stress (degree, duration, and interval of the elevated temperature) in humans (e.g., cryptorchidism, varicocele, and environmental heat exposure) is completely different compared to in vitro and in vivo animal experiments.
Keywords Heat stress • Oxidative stress • Reactive oxygen species • Spermatogenesis • Germ cells • Apoptosis • Thermotolerance • Heat-shock proteins
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