INTRATESTICULAR SPERMATOZOA RETENTION IN LOW FERTILITY AGING ROOSTERSIS RELATED TO MALFORMATIONS OF SERTOLI-CELL ECTOPLASMIC SPECIALIZATIONS

Citation
S. Weil et al., INTRATESTICULAR SPERMATOZOA RETENTION IN LOW FERTILITY AGING ROOSTERSIS RELATED TO MALFORMATIONS OF SERTOLI-CELL ECTOPLASMIC SPECIALIZATIONS, The Journal of experimental zoology, 275(4), 1996, pp. 317-325
Citations number
19
Categorie Soggetti
Zoology
ISSN journal
0022104X
Volume
275
Issue
4
Year of publication
1996
Pages
317 - 325
Database
ISI
SICI code
0022-104X(1996)275:4<317:ISRILF>2.0.ZU;2-N
Abstract
Fertility of domestic roosters kept under unnatural and constant condi tions, peaks to 96% at 32 weeks of age and subsequently declines rapid ly to 17% at 110 weeks of age. This decline in fertility is concomitan t with: (1) a reduction in the number and concentration of spermatozoa in ejaculates, and (2) an increment in the population of Sertoli cell -late spermatid complexes in seminiferous tubules. Impaired spermiatio n resulting in the retention of spermatozoa by Sertoli cells appears t o be the cause of the decline in fertility. We studied the relation be tween low fertility in ageing roosters and the status of Sertoli cell components, in particular those linked to spermatid disengagement, nam ely the ectoplasmic specializations surrounding the acrosomes. We foun d that the most prominent ultrastructural alterations of Sertoli cells in low (70 week) and in extremely low (110 week) fertility roosters w ere poorly formed actin-like filaments in the ectoplasmic specializati ons and the persistence of abundant secondary lysosomes. Other alterat ions included: (1) the reduction of cytoplasm volume and an increment in its electron-opacity; (2) the shortening of smooth endoplasmic reti culum strips; and (3) the appearance of more abundant, elongated mitoc hondria. We suggest that the ultrastructural modifications in Sertoli cells of low and extremely low fertility roosters are related to chang es in the hormonal profile which lead to the impairment (1) of spermia tion by severing the formation of actin-like filaments, resulting in s uperabundance of Sertoli cell-late spermatids complexes and, consequen tly, spermatozoa retention, and (2) cryptocrinal regulation of Sertoli cells causing the cessation of lysosomal cyclicity and, consequently, the accumulation of lysosomes. (C) 1996 Wiley-Liss, Inc.