Intratesticular spermatozoa retention

סוג הפרסום: מאמר בכתב עת
פורסם ע"י: אבי רוזנשטראוך , Weil, S., A.A. Degen, A. Rosenstrauch and M. Friedlander
שנת הוצאה: 1996
שם הספר/כתב העת: Journal of Experimental Zoology
שם המאמר: Intratesticular spermatozoa retention in low fertility ageing rooster is related to malformation of Sertoli cell ectoplasmic specializations
עמודים: 317-325
מספר גיליון: 275

Abstract

Fertility of domestic roosters kept under unnatural and constant conditions, peaks to 96% at 32 weeks of age and subsequently declines rapidly to 17% at 110 weeks of age. This decline in fertility is concomitant 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 spermiation resulting in the retention of spermatozoa by Sertoli cells appears to be the cause of the decline in fertility. We studied the relation between low fertility in ageing roosters and the status of Sertoli cell components, in particular those linked to spermatid disengagement, namely the ectoplasmic specializations surrounding the acrosomes.

We found that the most prominent ultrastructural alterations of Sertoli cells in low (70 week) and in extremely low (110 week) fertility roosters were poorly formed actin-like filaments in the ectoplasmic specializations and the persistence of abundant secondary lysosomes. Other alterations included: (1) the reduction of cytoplasm volume and an increment in its electron-opacity; (2) the shortening of smooth endoplasmic reticulum strips; and (3) the appearance of more abundant, elongated mitochondria.

We suggest that the ultrastructural modifications in Sertoli cells of low and extremely low fertility roosters are related to changes in the hormonal profile which lead to the impairment (1) of spermiation by severing the formation of actin-like filaments, resulting in superabundance of Sertoli cell-late spermatids complexes and, consequently, spermatozoa retention, and (2) cryptocrinal regulation of Sertoli cells causing the cessation of lysosomal cyclicity and, consequently, the accumulation of lysosomes.