Follicular Ability to Secrete Estradiol and Apoptotic DNA Fragmentation in a Hamster Model of Induced Follicular Atresia

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A model of induced follicular atresia consists of hypophysectomizing hamsters on the morning of estrus (day 1 of cycle) followed by injecting 30 IU equine chorionic gonadotropin (eCG). On the morning of day 4 (0 h) atresia is induced by administration of an antiserum to eCG (eCG-AS). One hour after eCG-AS, plasma estradiol and testosterone decline to 15.8% and 25.9%, respectively, of 0 h values with progressive decreases until at 12 h after eCG-AS, circulating estradiol is no longer detectable although baseline levels of testosterone (10.7%) are still present. The question raised was whether the simultaneous drop in both steroids at 1 h post eCG-AS is attributable to the fall in both hormones or to a more drastic decline in thecal androgens, thus depriving the granulosa of the precursors needed to synthesize estrogens. To answer this question, antral follicles were dissected 2 and 4 h after eCG-AS and incubated for 5 h, with or without the addition of 10 ng androstenedione. Addition of androgen at either time led to an increase in estradiol accumulation in the medium after the first hour which was sustained over the next 4 h. These experiments indicate that the immediate effect of eCG-AS is to sharply reduce thecal androgen production thus depriving granulosal aromatase of the necessary steroid substrate. In previous histological studies, we have shown that the earliest time when morphological signs of atresia are first discernable is by 4 h post eCG-AS as judged by pyknotic granulosa nuclei in the cumulus oophorus. In this study, using gel electrophoresis and autoradiography of 3’ labeled DNA followed by quantitating low and high molecular weight DNA, the earliest consistent onset of atresia was also at 4 h after eCG-AS.
日本繁殖生物学会の論文

Follicular Ability to Secrete Estradiol and Apoptotic DNA Fragmentation in a Hamster Model of Induced Follicular Atresia

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