346 



PHYSIOLOGY OF GONADS 



a weak androgen ; the second has no andro- 

 genic action. The protective effect possibly is 

 due to interference with the inhibiting action 

 of testosterone on pituitary gonadotrophin. 



XIV. Eflfeets of Altered Endocrine States 

 on the Testis 



Apart from the pituitary, alterations in 

 the endocrine system do not have pro- 

 nounced effects on the testis. The thyroid 

 has been studied extensively with regard to 

 testicular function (Maqsood, 1952). It is 

 difficult to generalize with respect to the 

 total impact of the thyroid on the testis 

 except to state that there is great variability 

 not only from species to species, but also in 

 different individuals of any one species. 

 Young, Rayner, Peterson and Brown (1952a) 

 suggested that the range of thyroid activ- 

 ity within which normal testicular function 

 is possible is rather wide. This may explain 

 why many effects on the testis of altered 

 thyroid function are marginal and why so 

 many reports are exceedingly conflicting. 

 Furthermore, it seems reasonable that ani- 

 mals having a naturally high level of thy- 

 roid activity may be impaired with respect 

 to reproductive performance when made 

 hypothyroid; conversely, species or indi- 

 viduals functioning normally at relatively 

 low levels of thyroid activity may be ad- 

 versely affected with regard to testicular 

 activity when made hyperthyroid (Young, 

 Rayner, Peterson and Brown, 1952b). 



In laboratory animals, hypothyroidism is 

 induced by thyroidectomy, by feeding of 

 antithyroid substances, by administering 

 radioiodine, or by combination of these 

 methods. Hyperthyroidism is induced by 

 feeding desiccated thyroid or various arti- 

 ficial thyroproteins, or by injecting thy- 

 roxine or triiodothyronine. Because it does 

 not seem to matter, as far as testicular 

 physiology is concerned, how hypothyroid- 

 ism and hyperthyroidism are induced, do- 

 tails of the method of altering thyroidal 

 status will not be given. 



Hypothyroid rats show decreased sper- 

 matogenesis and have smaller accessory 

 structures than normal rats (Smelser, 

 1939a). However, Jones, Delfs and Foote 

 (1946) found that adult hypothyroid rats 

 sire litters. Young animals, made hypothy- 

 roid at birth or shortlv thereafter, mav show 



delay in sexual maturation (Scow and Marx, 

 1945 ; Scow and Simpson, 1945) , or may have 

 normal reproductive tracts (Goddard, 1948). 

 Hyperthyroid rats show testicular degenera- 

 tion associated with a decrease in sperm pro- 

 duction and androgen secretion. The dele- 

 terious effects of hyperthyroidism are at- 

 tributed to an incapacity of the testis to 

 respond to gonadotrophin. The atrophy of 

 the accessory structures is attributed to the 

 decrease in androgen production and to 

 their increased requirement for androgen in 

 states of hyperthyroidism (Smelser, 1939b). 

 A nonendocrine explanation offered by 

 Cunningham, King and Kessell (1941) is 

 that testicular degeneration occurs because 

 of the increased body heat of the animals 

 in the hyperthyroid state. Richter and 

 Winter (1947), however, stated that hyper- 

 thyroidism has a stimulating effect on the 

 rat testis and accelerates the transfer of 

 sperm through the genital ducts. Lenzi and 

 Marino (1947) wrote that experimental hy- 

 perthyroidism causes a decrease in the num- 

 ber and volume of Leydig cells. Mixtures of 

 thyroxine and testosterone in doses that 

 have no effect on the rat testis when given 

 singly, produce severe atrophy in normal 

 rats (Masson and Romanchuck, 1945). 

 Small doses of testosterone augment the de- 

 bilitating effect of hyperthyroidism; large 

 doses protect the testis (Roy, Kar and 

 Datta, 1955). Changes in thyroidal status 

 also appear to affect the responsiveness of 

 the testis to gonadotrophins. Meites and 

 Chandrashaker (1948) stated that hyper- 

 thyroidism decreases the responsiveness of 

 the rat testis to exogenous gonadotrophin 

 (PMS) whereas hypothyroidism increases 

 it. The reverse holds for mice. 



In growing mice, sexual development is 

 retarded by hypothyroidism and accelerated 

 by mild liyperthyroidism (Maqsood and 

 R('inek(\ 1950). Moreover, the effectiveness 

 of testosterone on the seminal vesicles of 

 mice is increased by the concomitant ad- 

 ministration of thyroxine (Masson, 1947). 

 indicating an increased responsiveness of 

 the accessory reproductive tract to male 

 hormone in the hyperthyroid state. 



Hyperthyroid guinea pigs have small tes- 

 ticular tubules and fewer sperm in the semi- 

 niferous tubules. As in the rat, Richter 

 (1944) found that hyperthyroidism in the 



