Cryptorchidism is one of the most common abnormalities of male sexual development, and is characterized by the failure of the testis to descend into the scrotum. Despite extensive studies of
cryptorchidism over the past century, the mechanisms for temperature-induced germ-cell loss are not well understood. All of the main cell types in the testis are believed to be affected by the elevated testis temperature induced by
cryptorchidism. The cooler temperature in the special environment of the scrotum is required for maintaining optional conditions for normal spermatogenesis. Many studies reported that experimentally induced
cryptorchidism caused germ cell apoptosis and suppressed spermatogenesis. However, other factors including
hormones must also be examined for
cryptorchidism. To explore the mechanism for
cryptorchidism, in vitro cultures of testes have been used, but complete spermatogenesis using in vitro methods was not accomplished until 2011. In 2011, Sato et al. (Nature, 471, 504-507) reported the in vitro production of functional sperm in cultured neonatal mouse testes. Using this in vitro system, for the first time, we report that spermatogenesis was abrogated at 37 °C, in accordance with in vivo surgery-mediated
cryptorchidism, while spermatogenesis proceeded at 34 °C in cultured testes. This result clearly showed that temperature is the sole determinant of
cryptorchidism. Moreover, we found that spermatogenesis was arrested before early spermatocytes at 37 °C. In conclusion, using our in vitro system, we have demonstrated that (1) temperature is the determining factor for
cryptorchidism, and (2) higher temperature (37 °C) suppresses
DNA synthesis in spermatogenesis.