Yin Y, Stahl B C, DeWolf W C, Morgentaler A
Division of Urology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Apoptosis. 1998 Sep;3(4):281-7. doi: 10.1023/a:1009665309915.
Previous studies have demonstrated that testicular germ cell apoptosis can be induced both by heat stress and by withdrawal of androgens and gonadotrophins. To investigate whether heat-induced germ cell apoptosis occurs independently of the altered levels of hormones that occur with heat exposure, mouse testicular apoptosis was studied using an in vitro system with controlled levels of testosterone, FSH and LH. It was observed that cells underwent apoptosis sooner in the absence of hormones at the same temperature. Apoptosis also occurred earlier at abdominal temperature compared to scrotal temperature with the same hormonal levels. No somatic tissues studied underwent apoptosis at 37 degrees C under the same culture conditions. These results suggest that heat stress may independently activate an apoptotic pathway in the testis, and that hormone deprivation may induce apoptosis via a separate mechanism.
先前的研究表明，热应激以及雄激素和促性腺激素的撤除均可诱导睾丸生殖细胞凋亡。为了研究热诱导的生殖细胞凋亡是否独立于热暴露时发生的激素水平变化，我们使用了一个能控制睾酮、促卵泡激素（FSH）和促黄体生成素（LH）水平的体外系统来研究小鼠睾丸凋亡。结果发现，在相同温度下，缺乏激素时细胞更快发生凋亡。在相同激素水平下，腹部温度时的凋亡也比阴囊温度时更早发生。在相同培养条件下，37摄氏度时所研究的体细胞组织均未发生凋亡。这些结果表明，热应激可能独立激活睾丸中的凋亡途径，而激素剥夺可能通过一种独立机制诱导凋亡。
