HORMONAL-REGULATION OF SPERMATOGENESIS IN THE HYPOPHYSECTOMIZED RAT -QUANTITATION OF GERM-CELL POPULATION AND EFFECT OF ELIMINATION OF RESIDUAL TESTOSTERONE AFTER LONG-TERM HYPOPHYSECTOMY
Lr. Franca et al., HORMONAL-REGULATION OF SPERMATOGENESIS IN THE HYPOPHYSECTOMIZED RAT -QUANTITATION OF GERM-CELL POPULATION AND EFFECT OF ELIMINATION OF RESIDUAL TESTOSTERONE AFTER LONG-TERM HYPOPHYSECTOMY, Journal of andrology, 19(3), 1998, pp. 335-340
Spermatogenesis continues after long-term hypophysectomy (Hx), but mas
sive cell degeneration prevents seminiferous tubules from attaining th
e full complement of cells. One objective of this study was to determi
ne the vulnerable sites for completion of spermatogenesis in long-term
Hx rats. It is now known that Leydig cells continue to secrete small
amounts of androgen after Hx. A second objective was to determine the
cellular sites that are maintained by residual androgen secreted by Le
ydig cells post-Hx. Two groups of adult animals were utilized. Both gr
oups were Hx for 36 days, but one group of rats received the androgen
antagonist flutamide during the 26th through the 36th day of Hx (10 da
ys). Germ-cell numbers were quantified using a method that allowed the
ir expression as numbers of cells present per hour of development. In
the long-term Hx rat, the germ-cell population increased to preleptote
ne, but the divisions that led to preleptotene were inefficient due to
cell degeneration. Subsequent to preleptotene, there was a gradual lo
ss in cells such that there were few germ cells remaining by steps 9-1
3. Flutamide given to Hx rats did not result in a significant differen
ce in the numbers of intermediate and type B spermatogonia or signific
ant differences in progenitor cells. A significant and major depressio
n of cell numbers in Hx-fiutamide-treated rats occurred in the cell di
vision of type B spermatogonia to form preleptotene spermatocytes. The
re was a less dramatic, although significant, depression of cell numbe
rs in Hx-flutamide-treated animals that occurred from preleptotene unt
il late pachytene as well as an increased loss of round spermatids at
midcycle (Step 5-6). These data demonstrate that cell loss after long-
term Hx occurs at numerous phases of spermatogenesis. The data also de
monstrate that the presence of residual androgen action after long-ter
m Hx results in enhanced germ-cell survival. Although the major blocka
ge in cell viability occurs at midcycle steps in the long-term Hx rat,
there are several other hormone-sensitive phases of spermatogenesis.