344 



PHYSIOLOGY OF GONADS 



is nearly complete; only a few spermato- 

 cytes remain in addition to the Sertoli cells. 



The testis of the immature cat is un- 

 affected by estrogen (Starkey and Leathem, 

 1939j . Severe tubular atrophy and involu- 

 tion of the Leydig cells are noted in bulls 

 (Ferrara, Rosati and Consoli, 1953) and 

 boars (Wallace, 1949j after feeding with 

 stilbestrol. 



Although Haschek and Gutter (1951) 

 found no effect of estrogen on the testis, the 

 consensus is that any kind of estrogen pro- 

 duces profound involution of the human 

 testis. Temporary sterility is induced, of 

 course, as well as impotence and gyneco- 

 mastia (Heckel and Steinmetz, 1941). Most 

 of the information in man has been obtained 

 from the therapeutic administration of es- 

 trogen in cases of prostatic carcinoma 

 (Chome, 1956; de la Baize, Mancini and 

 Irazu, 1951 ; de la Baize, Bur, Irazu and 

 Mancini, 1953; de la Baize, Mancini, Bur 

 and Irazu, 1954; Schwartz, 1945; Schiiltz, 

 1952, to mention only a few) and from the 

 administration of estrogen to hypersexual 

 and homosexual men (Dunn, 1941). Estro- 

 gen induces atrophy of the tubules and the 

 Leydig cells ; the latter revert to fibroblasts. 

 The germinal epithelium shows an increase 

 in lipids and a decrease in glycogen. Unless 

 other disease is present, the atrophy pro- 

 ceeds so that only the Sertoli cells remain in 

 the tubules; even these cells may disappear 

 with the induction of peritubular hyaliniza- 

 tion and sclerosis. 



C. ADRENAL STEROIDS 



Tubular diameter in the testis of the 

 mature rat remains normal despite the pres- 

 ence of severe hypercortisonism resulting 

 fi'oiii administration of 3 mg. cortisone per 

 day for 6 weeks (Winter, Silber and Stoerk, 

 1950) or of 5 to 10 mg. per day (Ingle, 

 1950) . A few reports indicate that cortisone 

 stimulates growth of the testes of young 

 rats (Leroy, 1951) or causes degeneration 

 of the germinal ei)ithelium of the rat (Le- 

 roy, 1952) and mouse (Antopol, 1950). A 

 careful study by Hanson, Blivaiss and 

 Rosenzweig (1957) showed that the relative 

 growth of the testis is stimulated only 

 slightly by cortisone. 



Extremely little infoi-mation is avail- 

 able on the maintenance of spermatogenesis 



in hypophysectomized rats by cortisone. Le- 

 roy and Domm (1952) reported mainte- 

 nance at doses of 5 mg. per day. The Leydig 

 cells involuted, and the secondary sexual 

 apparatus was atrophic. However, these 

 findings were not confirmed by Aterman 

 ( 1956) , who used 5 mg. hydrocortisone per 

 day after hypophysectomy. The scrotum be- 

 came atrophic and the testes retracted. The 

 histologic appearance of the testes of the 

 cortisone-treated animals was indistinguish- 

 able from that of the hypophysectomized 

 controls. In rabbits Arambarri (1956) re- 

 ported only small changes in the relative 

 weight after prolonged use of cortisone. In 

 man, fairly large doses of cortisone given to 

 patients with rheumatoid arthritis do not 

 affect the histologic appearance of the testes 

 (Maddock, Chase and Nelson, 1953). Corti- 

 sone does bring about rapid testicular mat- 

 uration in boys who have congenital ad- 

 renal hyperjjlasia, but only if the bone age 

 is near the age of puberty (Wilkins and 

 Cara, 1954). This must not be construed 

 as a direct effect of cortisone on testicular 

 maturation. The action of cortisone in this 

 instance is to inhibit the excessive release 

 of corticotrophin (ACTH) from the pitui- 

 tary, thus reducing the amount of 17-keto- 

 steroids produced by the abnormal adrenals. 

 Removal of the inhibiting effect of the 

 androgenic steroids allow^s the formation of 

 gonadotrophin, with resulting maturation 

 of the testes. 



The consensus is that cortisone does not 

 cause any change in the histologic appear- 

 ance of the testis (Cavallero, Rossi and 

 Borasi, 1951 ; Soulairac, Soulairac and Teys- 

 seyre, 1955; Baumann, 1955). Furthermore, 

 it causes no change in the accessory struc- 

 tures, or in the secretion of androgen by the 

 testis. Cortisone has no direct effect on the 

 prostate or seminal vesicles in castrated ani- 

 mals (Moore, 1953). It is doubtful whether 

 cortisone can maintain spermatogenesis 

 after hypophysectomy. The bearing of these 

 studies on normal testicular physiologic 

 function is questionable. Cortisone has been 

 the main adrenal steroid studied in the rat 

 but the rat adrenal secretes corticosterone, 

 not cortisone. 



Desoxycorticosterone has been adminis- 

 tcicfl to rats in various doses. Arvy (1942) 

 and Overzici' (1952) I'cported that the de- 



