680 



PHYSIOLOGY OF GONADS 



spermatozoa after 9 days on an arginine- 

 deficient diet (Holt, Albanese, Shettles, 

 Kajdi and Wangerin, 1942). 



Adequate dietary protein cannot main- 

 tain reproductive function if the diet is 

 calorie deficient. Thus, a decrease in seminal 

 vesicle weight could be related to a decrease 

 in dietary calories while protein levels were 

 constant (Rosenthal and Allison, 1956). 

 However, the accessory gland weight loss 

 imposed by caloric restriction could be 

 slowed by increasing the dietary protein 

 (Rivero-Fontan, Paschkis, West and Can- 

 tarow, 1952). 



Alterations in testis function imposed by 

 inadequate protein are corrected when pro- 

 tein is returned to the diet at normal levels 

 (Aschkenasy and Dray, 1953). Neverthe- 

 less, the nutritional state of the animal as 

 a factor influencing recovery has been dem- 

 onstrated with stilbestrol-treated adult male 

 rats. While being fed an 18 per cent casein 

 diet, adult male rats were injected with 0.1 

 mg. stilbestrol daily for 20 days. Testis 

 weight decreased from 2848 to 842 mg., 

 spermatogenesis was abolished, and testis 

 water and protein content were significantly 

 reduced. Despite a reduction in food intake, 

 pair-fed controls exhibited no effect on re- 

 productive organs. When a protein-free diet 

 was substituted for the normal diet during 

 the administration of stilbestrol, atrophy of 

 the reproductive system was observed. Ces- 

 sation of hormone administration was fol- 

 lowed by a rapid return of testicular func- 

 tion toward normal when 18 per cent casein 

 was fed both during the injection period 

 and the recovery period. Within 30 days 

 spermatogenesis and testicular composition 

 were fully recovered. However, when 18 

 per cent casein was fed in the postinjection 

 period to rats that had received a protein- 

 free diet while being given stilbestrol, re- 

 covery was clearly slow. After a month, 

 spermatozoa were observed in only 30 per 

 cent of the testes and testis weight was sub- 

 normal. Despite the seeming similarity of 

 response by the two nutritional groups dur- 

 ing the injection period, the postinjection re- 

 covery on identical dietary intake revealed 

 marked differences in rate of recoverv (Lea- 

 them, 1958a). 



3. Fat 



Linoleic, linolenic, and arachidonic acids 

 are designated as essentially fatty acids, but 

 the physiologic role of these substances is 

 not clearly understood. Nevertheless, the 

 male reproductive organs are influenced by 

 dietary essential fatty acid levels. High 

 fat diets may enhance testicular weight 

 (Kaunitz, Slanetz, Johnson and Guilmain, 

 1956) whereas removal of fat from the diet 

 resulted in a degeneration of the seminifer- 

 ous tubules as evidenced by intracellular 

 vacuolation and a reduction in spermatids 

 and spermatozoa (Panos and Finerty, 

 1954). After 5 months of feeding a fat- 

 free diet, the rat testis may be devoid of 

 sperm (Evans, Lepkovsky and Murphy, 

 1934). Testis degeneration occurred despite 

 dietary supplements of vitamins A and E 

 and in animals whose health appeared quite 

 normal (Ferrando, Jacques, Mabboux and 

 Prieur, 1955; Ferrando, Jacques, Mabboux 

 and SoUogoub, 1955). 



Weanling rats fed 14 per cent arachis (pea- 

 nut) oil for 15 weeks exhibited a marked 

 impairment of spermatogenesis (Aaes-Jor- 

 gensen, Funch and Dam, 1956) and 28 

 per cent arachis oil induced testicular dam- 

 age of such an order that 15 weeks of feeding 

 ethyl linoleate did not restore fertility 

 (Aaes-Jorgensen, Funch and Dam, 1957). 



4. Vitamins 



Testicular dysfunction as judged by fail- 

 ure of sperm formation or atrophy of the 

 secondary sex organs has been observed in 

 deprivations of thiamine, riboflavin, pyri- 

 doxine, calcium pantothenate, biotin, and 

 vitamins A and E. One must distinguish, 

 however, between effects of inanition as- 

 sociated w^ith a vitamin deficiency and a 

 specific vitamin effect (Skelton, 1950) ; one 

 must also consider species differences (Bis- 

 kind, 1946). 



There is no question but that vitamin E 

 deficiency in the rat results in a specific 

 and irreversible damage to the testis. Tubu- 

 lar damage may proceed to the point where 

 only Sertoli cells remain and yet the in- 

 terstitial cells are not influenced (Mason, 

 1939). Similar changes followed vitamin E 

 deficiency in the guinea pig (Pappenheimer 

 and SchogolefT, 1944; Curto, 1954; Ingel- 



