NUTRITIONAL EFFECTS 



681 



man-Siindberg, 1954) , hamster (Mason and 

 Mauer, 1957), and bird (Herrick, Eide and 

 Snow, 1952; Lowe, Morton, Cunningham 

 and Vernon, 1957). However, little or no 

 effect of an absence of vitamin E was noted 

 in the rabbit (Mackenzie, 1942) and mouse 

 (Bryan and Mason, 1941), or in live stock 

 (Blaxter and Brown, 1952), or man (Lut- 

 wak-Mann, 1958), although vitamin E is 

 present in human testes (Dju, Mason and 

 Filer, 1958). Treatment of low-fertility 

 farm animals with wheat germ oil or to- 

 copherol or the use of this vitamin clinically 

 have provided only inconclusive results 

 (Beckmann, 1955) . Although some positive 

 effects have been reported in man, the re- 

 sults may be due in part at least to the spar- 

 ing action of tocopherol toward vitamin A. 



Vitamin A deficiency influences the testis 

 but changes are closely associated with the 

 degree of inanition. In the rat, a vitamin de- 

 ficiency sufficient to cause ocular lesions 

 did not prevent sperm formation, but a de- 

 ficiency of such proportions as to cause a 

 body weight loss did cause atrophy of the 

 germinal epithelium (Reid, 1949). Vitamin 

 A deficiency will induce sterility in mice 

 (McCarthy and Cerecedo, 1952). A gross 

 vitamin deficiency in bulls before expected 

 breeding age prevented breeding ; adult bulls 

 may exhibit a lower quality semen but they 

 remain fertile (Reid, 1949). Vitamin A de- 

 ficiency induces metaplastic keratinization 

 of the epithelium lining the male accessory 

 sex organs (Follis, 1948) and thus may in- 

 fluence semen. 



Testis damage induced by vitamin A de- 

 ficiency can be reversed, but vitamin A 

 therapy in man for oligospermia not due to 

 vitamin lack was without effect (Home 

 and Maddock, 1952) . 



Age of the animal and dosage are factors 

 which influence the results obtained in male 

 rats with administered vitamin A. Immature 

 male rats given 250 I.U. of vitamin A per 

 gram of body weight daily exhibited a loss 

 of spermatocytes, an effect which was ac- 

 centuated by tocopherol (Maddock, Cohen 

 and Wolbach, 1953). Little or no effect of 

 similar treatment was observed in adult 

 rats. The liver is the major storage depot 

 for vitamin A and the fact that the male rat 

 liver is more quickly depleted and less capa- 



ble of storage than is the liver of the female 

 should be considered in any attempted cor- 

 relation of the vitamin and hormone levels 

 (Booth, 1952). 



Other vitamin deficiencies have been 

 shown to influence the testis. A lack of 

 thiamine had little effect on testis weight, 

 but did influence the Leydig cells and pre- 

 vented growth of the accessory sex organs 

 (Pecora and Highman, 1953). A chronic 

 lack of ascorbic acid will cause a degenera- 

 tion of both Leydig cells and seminiferous 

 tubules. The effects of vitamin deficiency on 

 the testis has been distinguished from those 

 due to inanition and have been related to 

 changes in carbohydrate metabolism (Mu- 

 kherjee and Banerjee, 1954; Kocen and 

 Cavazos, 1958) . The importance of ascorbic 

 acid in the testis as related to function is 

 not evident, but concentrations of this vita- 

 min are maximal at 1 week of age (Coste, 

 Delbarre and Lacronique, 1953). 



Serious anatomic and functional impair- 

 ments of testes were noted in pantothenic 

 acid deficiency (Barboriak, Krehl, Cowgill 

 and Whedon, 1957), and development of 

 the rat testis and seminal vesicles was re- 

 tarded by a biotin deficiency (Bishop and 

 Kosarick, 1951; Katsh, Kosarick and Al- 

 pern, 1955), but the animals did not exhibit 

 marked alterations in other endocrine or- 

 gans (Delost and Terroine, 1954). Testos- 

 terone hastened the development of vitamin 

 deficiency and enhanced the severity of bio- 

 tin deficiency in both sexes, thereby sug- 

 gesting a hormone-vitamin relationship 

 (Okey, Pencharz and Lepkovsky, 1950). On 

 the other hand, testosterone had no effect on 

 the tolerance of mice for aminopterin, but 

 castration increased the tolerance (Goldin, 

 Greenspan, Goldberg and Schoenberg 1950). 



B. INFLUENCE OF NUTRITION ON THE EE- 



SPONSIVENESS OF MALE REPRODUCTIVE 



TISSUES TO HORMONES 



1. Testis 



a. Inanition. The testes of birds on limited 

 food intake were more responsive to hypo- 

 physeal gonadotrophin than fully fed birds 

 (Byerly and Burrows, 1938; Breneman, 

 1940). In the rat several investigators have 

 shown that the testis will respond to gonado- 

 trophin despite inanition (Moore and Sara- 



