Which Testicular Cells Are Vulnerable to Heat Stress

Basically, all testicular components are the target of heat stress. Quantitative analysis of changes in the seminiferous epithelium of rats exposed to local testicular heating indicates that primary spermatocytes are the most sensitive to damage by heat and that late spermatids are relatively resistant [ 36] . Oxidative stress is a major cause of heat stress in germ cells and leads to apoptosis [37-39]. Many recent studies in animals with experimental cryptorchidism or local testicular heating show that the process of spermatogenesis is exquisitely sensitive to temperature, with increased germ cell apoptosis (mostly spermatocytes and early spermatids) as a consequence of only relatively short periods of mild testicular heating [ 1,40,41]. Cataldo et al. found that the initiation of translation in pachytene spermatocytes and Sertoli cells is inhibited by exposure to abdominal temperature, and that elongated spermatids are much more resistant to heat stress [42], Needless to say, fetal testicular temperature is 37°C, which should be the same as the mother's temperature, and the cells which exist at birth, such as spermatogo-nia, Sertoli cells, and Leydig cells, should be considered to be resistant to heat stress. Actually, spermatogonia have a lower susceptibility to elevated temperatures [43], but abdominal temperature can markedly influence the number of sper-matogonial stem cells, especially type B spermatogonia, which will generate all the sperm in later life [44]. Of course, long-term exposure or higher temperatures may result in generalized damage to many different germ cell types [45] . Leydig cells and androgen secretion do not appear to be directly affected [1]. There are few experiments on the effects of elevated environmental temperature on the secretion of hormones that control reproductive functions. In vitro and in vivo experiments about the effect of heat and oxidative stress suggest harmful effects on hormonal secretion [46, 47],

A controversial issue is whether ejaculated spermatozoa can be damaged by heat stress when deposited in the reproductive tract, because the temperature of the female reproductive tract is basically 37°C. When cultured at 40°C, the fertilizing capability of bull spermatozoa and the competence of the resultant embryos to develop to the blastocyst stage were not altered [48]. On the other hand, reduced mouse litter sizes were reported after males were subjected to a variety of heat stress regimens. For example, in vitro fertilization using sperm from testes heated 7 days before sperm harvest (an epididymal or late spermatid effect of heating) showed reduced numbers of embryos developing from the 4-cell stage onwards, and those from testes heated 21 days earlier (a spermatocyte effect) showed reduced numbers of embryos developing from the 2-cell stage onwards [49]. A further study focusing on the effects of increased whole body temperature by exposing male mice twice to 36°C for 12 h on each occasion showed reduced sperm number, pregnancy rate, and litter size with maximum effects observed 10 or 14 days after exposure to heat stress [3]. In the study by Rockett et al., control females that were mated with males subjected to transient, acute (20 min), scrotal heat stress 23-28 days previously resulted in reduced litter sizes, consistent with an effect on spermatocytes [6] . Other studies showed that heat stress affects fertility in mice and reduces pregnancy rate and embryo weight as well as fertilization rate in vitro, when sperm from males subjected to heat stress were used [5] , Even if cell death is not observed, sperm cell membrane and DNA are susceptible to heat-induced oxidative stress, and the tes-ticular components undergo cell cycle arrest and thermotolerance, which are described in the following sections.

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