Hadziselimovic F, Girard J
Horm Res. 1977;8(2):76-83. doi: 10.1159/000178783.
Cryptorchidism was induced experimentally by treating pregnant mice on the 14th day of pregnancy with 5 mg estrogen. Testes from cryptorchid and control newborn and adult mice were investigated with radioimmunoassay and electron microscopy. It was concluded that a normal Leydig cell function plays a decisive role in testicular descent. In cryptorchidism, Leydig cells at birth are atrophic. Testicular testosterone content is diminished as compared to controls. Ultrastructural alterations of Leydig cells observed in our experiments closely resemble those found in biopsies of cryptorchid patients. In male mouse offspring, prenatal estrogen injection induced not only a cryptorchidism but also Leydig cell atrophy and a permanently impaired function. Testosterone content is still significantly diminished after puberty. It is proposed therefore that an insufficiency of endocrine gonadal function of hypothalamo-pituitary origin occurring during intrauterine development is one of the main causes of cryptorchidism. An appropriate long-term therapy could diminish the high sterility rate.
通过在怀孕第14天给怀孕小鼠注射5毫克雌激素来实验性诱导隐睾症。用放射免疫测定法和电子显微镜对隐睾症小鼠以及对照新生小鼠和成年小鼠的睾丸进行了研究。得出的结论是，正常的睾丸间质细胞功能在睾丸下降中起决定性作用。在隐睾症中，出生时的睾丸间质细胞萎缩。与对照组相比，睾丸睾酮含量降低。在我们的实验中观察到的睾丸间质细胞超微结构改变与在隐睾症患者活检中发现的非常相似。在雄性小鼠后代中，产前注射雌激素不仅会导致隐睾症，还会导致睾丸间质细胞萎缩和功能永久性受损。青春期后睾酮含量仍显著降低。因此，有人提出，子宫内发育期间发生的下丘脑 - 垂体源性性腺内分泌功能不足是隐睾症的主要原因之一。适当的长期治疗可以降低高不育率。
