Effects of cryptorchidy, parabiosis, and estrogen administration upon Leydig cell tumorigenesis in Fischer rats.

The effects on Leydig cell tumorigenesis of surgical cryptorchidy, parabiotic union with a castrate male partner, and a combination on the two procedures as well as of the continuous exposure to a high level of diethylstilbestrol stimulation were studied in the high-tumor Fischer rat. Localized foci of adenomatous hyperplasia were found to have developed in the scrotal testes of most animals by 13.5 months of age. Parabiosis with a castrate male partner did not appear to alter the process significantly, but surgical cryptorchidy, even when combined with parabiosis, completely prevented the development of this pretumorous lesion as did the chronic administration of diethylstilbestrol. Furthermore, intraabdominal residency throughout the life span of animals was found to inhibit Leydig cell tumor formation almost completely. Comparative end organ weights as well as plasma testosterone determinations reported earlier indicated that, with continued intraabdominal residency 3 months and longer, the Leydig cells in this strain of rat became significantly less responsive to stimulation by pituitary gonadotropic hormones. The data are interpreted as indicating that the endocrine stimuli most centrally involved in the genesis of this tumor type are quite different in the mouse and the rat, an abnormal response to gonadotropic stimulation being pivotal in the rat while reaction to estrogens is the most significant factor in the mouse.