MAMMALIAN TESTIS 



343 



1 





■•■A 





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Fig. 5.22. Elluci ul iC5io.stcruiie on the testis of a man with infertiUty caused by adult 

 tubular failure. Testicular biopsies, showing the pronounced degree of sclerosis and hyaliniza- 

 tion that occurs when an initially very poor testis is subjected to the administration of 91 

 consecutive injections of testosterone propionate, 25 mg. each. A, before treatment; B, at 

 end of 91 days of treatment; C, 17 months after cessation of treatment. Note, in C, the 

 disappearance of hyalinization, the increase in size of the seminiferous tubules, and the 

 appearance of fairly orderly spermatogenesis. Leydig cells, not shown here, were present 

 17 months after treatment was stopped. (From C. G. Heller, W. O. Nelson, I. B. Hill, 

 E. Henderson, W. O. Maddock, E. C. Jungck, C. A. Paulsen and G. E. Mortimore, Fertil & 

 Steril., 1, 415, 1950.) 



testosterone. The mechanism by which gon- 

 adotrophin is inhibited always has been 

 assmned to be a direct effect of androgen on 

 the pituitary. It is interesting in this regard 

 that Paulsen (1952) showed that the use of 

 testosterone, w^iile reducing urinary gonado- 

 trophin, increases the amount of urinary 

 estrogen 20-fold. Estrogen is by far the 

 most powerful suppressant of gonadotrophin 

 secretion known; hence, it is possible that 

 the atrophy of the testis observed during 

 testosterone therapy in man may be caused 

 by estrogen. No reports of maintenance of 

 spermatogenesis in men with pituitary in- 

 sufficiency or after hypophysectomy are 

 available. 



B. ESTROGENS 



Various natural and synthetic estrogens 

 have been given to rats, guinea pigs, ham- 

 sters, cats, bulls, boars, and man. In all 

 forms, estrogen induces atrophy of the male 

 gonad. The histologic appearance of the 

 atrophic rat testis after estrogen therapy 

 has been described by Dischreit (1940). In 

 young rats, estradiol prevents testicular 

 descent, produces atrophy, and inhibits 

 spermatogenesis (Pallos, 1941; Gardner, 

 1949). Two weeks following atrophy in- 

 duced by estradiol or stilbestrol, regenera- 

 tion of the testis begins (Bourg, Van Meen- 



sel and Compel, 1952) and is complete 

 wuthin 6 weeks (Lynch, 1952). However, 

 Snair, Jaffray, Grice and Pugsley (1954) 

 noted that the accessory sex organs re- 

 cover before spermatogenesis resumes. The 

 same inhibiting effects have been obtained 

 with methylbisdehydrodoisynolic acid 

 (Tuchmann-Duplessis and Mercier-Parot, 

 1952) and hydroxypropiophenone (Lacas- 

 sagne, Chamorro and Buu-Hoi", 1950). In 

 general the effect of estrogen in the rat is 

 to induce atrophy of the Leydig cells and 

 germinal epithelium, so that only sperma- 

 tocytes, spermatogonia, and Sertoli cells 

 remain. 



Uncertaint3^ exists concerning the general 

 effects of estrogen in guinea pigs. Lynch 

 (1952) noted that the Leydig cells are nor- 

 mal in animals treated with estrogen, but 

 Marescaux (1950) and Chome (1956) noted 

 that the Leydig cells are atrophic. Mares- 

 caux, in studying hypophysectomized guinea 

 pigs, concluded that estrogen has a direct 

 stimulating effect on the Leydig cell. Mas- 

 sive tubular damage occurs in the guinea 

 pig after administration of estrogen. In the 

 hamster. Bacon and Kirkman (1955) found 

 that various estrogens induce testicular 

 atrophy. In occasional animals, hyperplasia 

 of interstitial and Sertoli cells occurs and is 

 attributed to direct effects of estrogen. In 

 general, atrophy of the germinal epithelium 



