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kills cells in S phase at the time of administration (de Rooij et al. 1985 ). This drug
also kills spermatogonia in S phase and in epithelial stage VIII it will kill all A1
spermatogonia in a particular area because these cells synchronously go through S
phase in stage VIII. As a result of the disappearance of the A1 spermatogonia from
tubule areas in stage VIII at the time of ARA-c administration, particular stretches
of the seminiferous tubules will not contain any differentiating type spermatogonia
during the ensuing epithelial cycle. In contrast, very few A s,pr,al spermatogonia go
through S phase in stage VIII. As a result of this, the areas emptied from A1 sper-
matogonia will have a virtually normal complement of A s,pr,al spermatogonia. By
following these particular areas with time after administration of Ara-C, one can
study the proliferative behavior of the A s,pr,al spermatogonia in a situation in which
they are not surrounded by differentiating spermatogonia. Interestingly, in such a
situation the proliferative activity of the cells is not inhibited around stage II and
very much larger numbers of A1 spermatogonia are produced (Fig. 4.6 ) (de Rooij
et al. 1985 ). Previously, in the mouse it was found that when more than about 50%
of the spermatogonia are killed by administration of busulfan, there is an enhanced
proliferation of A s,pr,al spermatogonia, findings compatible with these results (van
Keulen and de Rooij 1974 ). Together, these results confirm and expand the notion
that came forward from the chalone work, i.e., that differentiating spermatogonia
Fig. 4.6 Comparison between the numbers of cells produced by A s , A pr , and A al spermatogonia
during the cycle of the seminiferous epithelium in an area from which the generation of differenti-
ating spermatogonia has been removed and cell production in the normal epithelium of the Chinese
hamster. More cells are produced when no differentiating spermatogonia are present indicating that
these cells inhibit A s,pr,al spermatogonial proliferation. Data from de Rooij et al. ( 1985 )
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