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Abstract
Gonadotropin-releasing hormone (GnRH) analogs: agonists
(GnRH-a) or antagonists (GnRH-ant) have been widely used
to inhibit gonadotropin pituitary release. Besides the
effect of GnRH analogs on the pituitary-gonadal axis,
studies have shown that GnRH has extrapituitary effects,
particularly on the rat and human ovary. In the present
study, we have evaluated the direct in vivo effects of the
GnRH-a: Leuprolide Acetate (LA) and/or the GnRH-ant:
Antide (Ant) on ovarian follicular development in
prepuberal eCG-treated rats. LA significantly decreased
while Ant increased ovarian weight compared to control,
however co-injection of both compounds had no effect. In
addition, LA increased the number of preantral follicles
(PF) and atretic follicles (ATF) and decreased the number
of early antral (EAF) and preovulatory follicles (POF).
The co-injection of Ant interfered with this LA effect.
Ant alone increased the number of POF compared to control.
Analysis of apoptosis has shown that LA increases the
percentage of apoptotic cells in PF, EAF and POF; however,
Ant prevented this effect. In addition, Ant alone
decreased the percentage of apoptotic cells in EAF and
POF. Data have shown that Ant per se inhibited BAX
translocation from cytosol to mitochondria and retained
cytochrome C in the mitochondria while LA induced
cytochrome C release. We concluded that Ant inhibits the
apoptosis in preovulatory follicles through a decrease of
BAX traslocation to mitochondria, suggesting that GnRH may
act as a physiological intraovarian modulator factor able
to interfere with the follicular development through an
increase in apoptotic events mediated by an imbalance
among the BCL-2 family members.
Key words:
Ovary •
Apoptosis •
Follicle •
Gonadotropin-releasing hormone
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