Effect of dietary selenium and vitamin E on spermatogenic development in boars.

An experiment involving a total of 61 crossbred boars evaluated the effects of dietary Se and vitamin E on spermatogenic development at various stages of sexual development and the prostaglandin F2alpha (PGF2alpha) content in the seminal vesicle and prostate glands at 18 mo of age. The experiment from 5.4 to 9 mo of age was conducted as a 2 x 2 factorial in a randomized complete block design. Dietary Se at 0 or .5 ppm was the first factor and vitamin E at 0 or 220 IU/kg diet was the second. From 9 to 18 mo of age, a group of sexually active and inactive boars was a third factor. Treatment diets were fed from weaning (28 d of age) to the end of the experiment. Three boars per treatment group at 5.4 (105 kg BW), 6.2 (130 kg BW), and 9.0 (150 kg BW) mo of age were killed and the testes collected. From 9 to 18 mo of age, three boars from each dietary treatment group were used for semen collection, and another set of three to four boars from each treatment group remained sexually inactive. At 18 mo, both sets of boars were killed and their testes, prostates, and seminal vesicles were collected. The testis at each age was evaluated for sperm reserve numbers and germ and Sertoli cell populations. At 5.4 or 6.2 mo of age, testicular sperm reserves were not affected by dietary Se (P > .15), at 9.0 mo of age there was a trend for a higher (P < .10) number of sperm reserves, and by 18 mo of age the Se-fed boars had higher (P < .01) numbers of sperm reserves. Vitamin E had no effect (P > .15) on testicular sperm reserves at any age period. Boars fed dietary Se had a greater number of Sertoli cells (P < .01) and round spermatids (P < .01) at 6.2 mo of age, but by 18 mo of age the boars fed Se had more Sertoli cells (P < .05), more secondary spermatocytes (P < .01), and more round spermatids (P < .05). Vitamin E did not affect Sertoli or germ cell populations at the various ages. Boars at 18 mo of age had lower PGF2alpha concentrations in the prostate (P < .05) and seminal vesicles (P < .01) when vitamin E was fed, whereas Se had no effect. Sexually active boars had lower PGF2alpha concentrations in the seminal vesicles (P < .01) than sexually inactive boars, but there was no effect (P > .15) of sexual activity on the number of Sertoli cells, primary or secondary spermatocytes, or round spermatids. Our results indicate that Se has a role in establishing the number of boar spermatozoal reserves and Sertoli cells, whereas supplemental vitamin E did not affect these criteria.