A molecular basis for estrogen-induced cryptorchidism

被引:158
作者
Nef, S [1 ]
Shipman, T [1 ]
Parada, LF [1 ]
机构
[1] Univ Texas, SW Med Ctr, Ctr Dev Biol, Dallas, TX 75390 USA
关键词
Insl3; RLF; Ley I-L; cryptorchidism; estradiol; Estriol; DES; gubernaculum;
D O I
10.1006/dbio.2000.9785
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Male sexual differentiation relies upon testicular secretion of the hormones testosterone, Mullerian inhibiting substance, and insulin-3 (Insl3). Insl3 is responsible for testicular descent through virilization and outgrowth of the embryonic gubernaculum. In mouse, prenatal exposure to 17 beta-estradiol and the nonsteroidal synthetic estrogen diethylstilbestrol (DES) disturbs the endocrine balance, causing demasculinizing and feminizing effects in the male embryo, including impaired testicular descent (cryptorchidism). In the current study, we show that maternal exposure to estrogens, including 17 alpha- and beta-estradiol, as well as DES, specifically down regulates Insl3 expression in embryonic Leydig cells, thereby providing a mechanism for cryptorchidism. These experiments may have implications for the widespread use of estrogenic substances in agriculture and the environment. (C) 2000 Academic Press.
引用
收藏
页码:354 / 361
页数:8
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