1108 



SUBMAMMALIAN VERTEBRATES 



of nicotinic acid and of riboflavin may be 

 that testosterone is not inactivated in the 

 liver of these deficient birds. Evidence that 

 these two vitamins are involved in the 

 inactivation of estrogen (Singher, Kensler, 

 Taylor, Rhoads and Unna, 1944; DeMeio, 

 Rakoff, Cantarow and Paschkis, 1948) sug- 

 gests that they may also be involved in the 

 inactivation of testosterone. Such impair- 

 ment of inactivation would result in high 

 circulating testosterone levels. Evidence that 

 would indicate whether or not vitamin E de- 

 ficiency impairs liver function of chickens 

 is not available, as far as I have been able to 

 find, nor is evidence that vitamin E is 

 involved in steroid hormone inactivation. 

 Thus, the increased comb response to andro- 

 gen in vitamin E deficiency may not with 

 certainty be ascribed to effects of the vita- 

 min on liver enzyme systems. 



The effect of folic acid deficiency on 

 testicular development and on the comb re- 

 sponse to androgen has been investigated 

 in experiments in which inanition effects 

 were separated from specific folic acid ef- 

 fects by the paired feeding technique (Zar- 

 row, Koretsky and Zarrow, 1951). The con- 

 clusion was that folic acid deficiency did 

 not affect testes size of cockerels but that 

 it did increase comb response to a standard 

 dose of androgen. The latter was postulated 

 to be the result of impaired inactivation of 

 the testosterone by the liver. 



8. Drugs 



Brief mention has to be made of the 

 effect of different drugs on testicular de- 

 velopment. Some of these effects were first 

 noted when the drugs were incorporated in 

 poultry feeds to combat various diseases. 



Enheptin (2-amino,5-nitrothiazole) in- 

 hibits testicular and comb development, 

 probably by inhibiting pituitary gonado- 

 trophin secretion (Pino, Rosenblatt and 

 Hudson, 1954). This conclusion is based on 

 the lowered gonadotrophin content found in 

 the pituitary of Enheptin-treated cockerels 

 and also on the normal testicular develop- 

 ment obtained after gonadotrophin treat- 

 ment of Enheptin-fed cockerels. The re- 

 lated drug, 2-acetylamino-5-nitrothiazole, 

 caused only slight, localized areas of at- 



rophy of the seminiferous tubules and an 

 accompanying decrease in semen volume 

 without an effect on fertilitv (Cooper and 

 Skulski, 1957). 



Sulfamethazine, a coccidiostat, causes 

 precocious testicular and comb development 

 of cockerels (Asplin and Boyland, 1947) 

 probably by way of an effect on the thyroid. 

 Increased thyroid size with normal histology 

 and normal P^^ uptake per mg. thyroid led 

 to the conclusion that sulfamethazine feed- 

 ing caused slight hyperthyroidism (van Ti- 

 enhoven, Thomas and Dreesen, 1956). 



Nicarbazin, another coccidiostat which in- 

 hibits egg production (Baker, Hill, van 

 Tienhoven and Bruckner, 1957) , has no ap- 

 parent effect on testicular size, semen char- 

 acteristics, or fertility (van Tienhoven, 

 Crawford and Duchaine, 1957). 



Furazolidone .V- (5-nitro-2-furfurylidene) 

 -3-amino-2-oxazolidone, fed at a level of 

 0.011 per cent of the feed to combat Sal- 

 monella and Histomonas infections, delayed 

 sexual maturity of turkey males. Apparently 

 there is great variability in the response to 

 this drug, for 4 of 30 males had not yielded 

 any semen at 296 days of age, whereas the 

 average age for the first ejaculate for the 

 other 26 toms was 208 days, only one week 

 later than the controls (Redman and Smyth, 

 1957). Cooper and Skulski (1955) noted 

 that feeding of this drug (0.022 per cent of 

 the feed) caused a marked decrease in tes- 

 ticular size at 12 weeks of age. The lack 

 of an effect noted when either 0.011 or 

 0.022 i)er cent furazolidone was fed to 0- 

 to 4-week-old cockerels (Francis and Shaff- 

 ner, 1956) may have been a result of the 

 younger age. If this drug interferes with the 

 later stages of spermatogenesis, no difference 

 would be noticeable at 4 weeks of age. 



The mode of action, whereby the drug 

 interferes with male reproduction, has not 

 been established. 



In general, our knowledge of the effect of 

 nutrition and of pharmacologic agents on 

 avian male reproduction is fragmentary 

 compared with our knowledge of the same 

 subject in mammals, although the rooster 

 should be a good experimental animal for 

 studying the interaction between metabolic 

 factors and the functioning of the testis. 



