الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
The present study was designed to examine whether cetrorelix as
GnRH-ant has potential protective effect aganist ɤ-radiation-induced
ovarian dysfunction in vivo by studying its effects on folliculogenesis,
different markers of OS, proliferation, apoptosis, and angiogenesis in
an experimental model of ɤ-radiation-induced ovarian failure in rats.
The study was designed as follows:
Animals (total no.=100) were divided randomly into four groups
(group=25) and were either exposed to a single dose of ɤ-radiation (3.2
Gy) and/or treated with cetrorelix s.c. (0.5 mg/kg) once daily for ten
days.
The following parameters were investigated:
A. Assessment of serum AMH, E2, and FSH level.
B. Morphometric analysis of ovarian follicles type and number.
C. Histopathological examination: H&E used for routine histological
examination of ovarian tissues.
D. Assessment of OS markers: ovarian content of GSH and MDA, in
addition to GPx and GRx activities.
E. Assessment of Apoptotic markers: ovarian expressions of
cytochrome c and caspase 3 and BAX/BCL-2 ratio.
F. Assessment of proliferative marker (PCNA).
G. Assessment of Angiogensis: ovarian VEGF expression.
The results of the present study can be summarized as follows:
1. The current study demonstrated that endocrine environment was
affected by radiation, as shown by a drastic increase in FSH levels and
a significant decrease in AMH and E2 levels. Additionally, as a result
of the early depletion of primordial follicles, irradiated females
displayed POF. On the other hand, treatment of female rats with
cetrorelix corrected the change in AMH, E2, and FSH levels caused by
radiation.
2. The number of primordial follicles may have reached such a critical
value that the mechanisms controlling recruitment of primordial
follicles into the growing pool could not be effective in the irradiated
ovaries. As a result, we have demonstrated that whole-body irradiation
with a single dose of 3.2 Gy induced a depletion of the growing preantral
follicles within a time period of 24 h, with marked reduction in
GCs proliferation. In contrast, cetrorelix pre-treatment of the irradiated
rats for 10 days preserved ovarian follicles’ stock and increased PCNA
expression of the irradiated ovaries.
3. Histopathological examination using H&E stain showed that the
stromal tissue of the irradiated ovaries occupied most of the ovarian
structure which was characterized by severe hemorrhage with very few
primordial follicles were detected at the periphery of the ovary.
Curiously, treatment of rats with cetrorelix preserved ovarian tissues
from radiation-induced hemorrhage and degeneration.
4. Regarding the OS, radiation exposure resulted in a significant
increase in ovarian MDA accompanied with a significant depletion of
GSH levels as well as GPx and GRx. activities. However, cetrorelix
treatment of the irradiated rats significantly reduced the radiationinduced
production of ROS and inhibited subsequent lipid
peroxidation marker (MDA).
5. Rats exposure to irradiation resulted in an increased ovarian and
theca cells as well as ovarian epithelial cells apoptosis as evidenced by
increased cytochrome c, caspase 3 expression, BAX/BCL-2 ratio.
6. Cetrorelix treatment for ten days of the whole body irradiated rats
significantly diminished such apoptosis-induced.
7. Rats exposure to irradiation resulted in an increased angiogenesis
(VEGF). However; cetrorelix treatment of the irradiated rats
significantly reduced the radiation-induced production of VEGF.