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Department of Experimental Radiation Oncology, University of Texas M. D. Anderson Cancer Center (G.A.S., G.S., G.W., M.L.M.), Houston, Texas 77030; the Department of Cell Biology, University of Utrecht (D.G.R.), 3584 CX Utrecht, The Netherlands; the Department of Physiology, University of Turku (I.H.), 20520 Turku, Finland; Central Research and Development ASTA Medica AG. (T.R.), D-60314 Frankfurt Aim Main, Germany; and the Department of Physiology, Southern Illinois University (L.D.R.), Carbondale, Illinois 62901
Address all correspondence and requests for reprints to: Dr. Gladis A. Shuttlesworth, Department of Experimental Radiation Oncology, University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030. E-mail: shuttles{at}utmdacc.mdacc.tmc.edu
The initial changes in the numbers, proliferation, and differentiation
of A spermatogonia in irradiated rats after the administration of a
GnRH antagonist, which is known to induce differentiation in this
system, were investigated. LBNF1 rats were given 6 Gy of
-irradiation; some were treated with the GnRH antagonist Cetrorelix
beginning 15 weeks after irradiation. Although the spermatogonia in the
irradiated rats without hormone treatment continue to proliferate
(labeling and mitotic indexes of 24% and 18%, respectively), they
underwent apoptosis (apoptotic indexes of 21% by the terminal
transferase-mediated end labeling assay and 9% by nuclear morphology),
resulting in a constant number of A spermatogonia. Whole mount analysis
of clones of A spermatogonia revealed that larger clones were more
likely to undergo apoptosis than mitosis. Hormone administration
decreased the intratesticular testosterone concentration to 6% of the
level in irradiated rats within 1 week. Concomitantly, there was a
decrease in spermatogonial apoptotic indexes to 43% of levels in
irradiated-only rats, leading to an increases in their numbers by
150%, their diameters by 11%, and their labeling indexes by 31%. The
sizes of the mitotic clones gradually increased, and clones of more
than eight cells appeared at week 3 of hormone treatment. A
spermatogonial differentiation began at week 4, and by week 6.6,
differentiation occurred in 30% of the tubules. Thus, suppression of
intratesticular testosterone by the GnRH antagonist may be responsible
for the immediate changes in spermatogonial numbers and kinetics, but
several additional steps are required before differentiation begins,
which did not occur until week 4.
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