352 



PHYSIOLOGY OF GONADS 



why the testes occupy the scrotum. The ex- 

 planation that scrotal residence provides 

 "optimal testicular temperature" is not sat- 

 isfying because one then wishes to know 

 why the male gonad requires the cooler en- 

 vironment afforded by the scrotum. Failure 

 of the testes to descend may occur as a 

 consequence of defects in the testes, prob- 

 ably of genie origin ; or because of anatomic 

 obstacles, representing embryologic defects, 

 inadvertently placed along its prescribed 

 narrow path. In either event, the testis is 

 damaged, mildly in its endocrine function, 

 and seriously in its spermatogenic function. 

 Impairment of spermatogenesis of the 

 misplaced testis is due to the relatively high 

 temperature of the abdomen. Temperature 

 affects the germinal epithelium directly. It 

 also affects the testis indirectly through the 

 circulatory system. The effect of tempera- 

 ture, or for that matter, of any type of in- 

 jurious agent whether it be chemical or 

 physical, is atrophy of the seminiferous 

 epithelium. The response of the germinal 

 tissue to deprivation of pituitary gonado- 

 trophin likewise is atrophy. Quantitative 

 variation among different species does of 

 course exist, but qualitatively, atrophy is 

 the universal response to injury. Obviously, 

 a common denominator must exist for this 

 fairly general reaction on the part of the 

 germinal epithelium. If various chemical 

 and physical stimuli act on the testis by 

 means of suppression or interference with 

 the action of gonadotrophins, atrophy of 

 the Leydig cells would also result. However, 

 many chemical and physical agents affect 

 only the germinal epithelium, leaving the 

 Leydig cells unscathed. Thus, the germinal 

 epithelium can be damaged directly and 

 the variable damage to the components of 

 the spermatogenic epithelium must be due 

 to different sensitivities of its cellular com- 

 ponents. The Sertoli cell is much more re- 

 sistant than the cells of the germinal line, 

 and of the seminiferous elements, the type 

 A spermatogonia are the most resistant. Of 

 great importance in the interpretation of 

 the damage induced by many substances or 

 occurring as a result of disease is the char- 

 acteristic of the germinal epithelium to 

 reproduce in a fixed order and sequence. It 

 follows that the extent of injury to sper- 

 matogenesis as a whole would 1)C determined 



by the relative susceptibility of the various 

 germinal cells as well as by the nature of 

 the noxious agent. If only sperm cells are 

 affected, spermatogenesis will proceed 

 through the formation of spermatid. How- 

 ever, if spermatogonia are injured, full dif- 

 ferentiation of the germinal epithelium will 

 fail, and only Sertoli cells will be found in 

 the tubule. Thus, it is possible that all sorts 

 of injury to the testis, if sufficiently great, 

 may result in the same end stage of tes- 

 ticular atrophy. In spite of this common 

 reaction pattern to severe injury, many sub- 

 stances induce what seem to be specific le- 

 sions in the testis. However, these represent 

 intermediate or partial injuries, and do not 

 necessarily constitute exceptions to the gen- 

 eral pattern of testicular response to injury. 

 As more is learned about the biochemistry 

 of the germinal epithelium, it may be pos- 

 sible to induce specific lesions. 



Quantitative studies on spermatogenesis 

 have greatly clarified the role played by 

 the pituitary gland. Spermatogenesis does 

 proceed in hypophysectomized animals but 

 only at a low rate. Also it appears that an- 

 drogen, not gonadotrophin, is responsible 

 for the maturation of the spermatid. How- 

 ever, it must be remembered that the forma- 

 tion of androgen is dependent on pituitary 

 gonadotrophic function. Thus spermato- 

 genesis is regulated entirely by pituitary 

 gonadotrophins, which exert direct super- 

 vision over the rate of the mitotic and 

 meiotic activity of germ cells and indirect 

 supervision by way of the Leydig cell over 

 spermatid maturation, or spermiogenesis. 

 The effectiveness of androgen in sperm for- 

 mation is hardly equal to that of the pitui- 

 tary. Addition of trophic hormones (except 

 gonadotrophin) or of hormones of the target 

 glands (tliyi'oid, adrenal cortical hormone, 

 etc. I will ])robably not improve the ef- 

 fectiveness of androgen. The best evidence 

 that this surmise may be correct is obtained 

 from jnitients with hypogonadotroi)hic hy- 

 l)ogonadism. These i)atients have normal 

 function with respect to the other trophic 

 hormones of the pituitary and, therefore, 

 normally functioning peripheral glands, but 

 do not have sperm. 



The quantitative studies on the spermato- 

 genic cycle have important bearing on other 

 |)i'o]»lciiis wliicli have been i)uzzling to endo- 



