HORMONAL-REGULATION OF SPERMATOGENESIS IN THE HYPOPHYSECTOMIZED RAT -CELL VIABILITY AFTER HORMONAL REPLACEMENT IN ADULTS AFTER INTERMEDIATE PERIODS OF HYPOPHYSECTOMY
A. Elshennawy et al., HORMONAL-REGULATION OF SPERMATOGENESIS IN THE HYPOPHYSECTOMIZED RAT -CELL VIABILITY AFTER HORMONAL REPLACEMENT IN ADULTS AFTER INTERMEDIATE PERIODS OF HYPOPHYSECTOMY, Journal of andrology, 19(3), 1998, pp. 320-334
A quantitative analysis of germ-cell populations in normal, hypophysec
tomized (Hx), and Hx-hormone-treated animals was undertaken during per
iods of regression that were characterized as intermediate, between sh
ort-term and long-term regression of the testis. Twenty-one groups of
adult rats were administered either follicle-stimulating hormone (FSH)
, growth hormone, thyroid-stimulating hormone (TSH), or testosterone (
T) in various doses and combinations. The dosage of T administered was
less than that expected to achieve maximum testis weight. Flutamide a
nd Casodex were used to compete with androgen binding to receptors in
Hx animals, as it is known that small amounts of androgen are secreted
in the absence of pituitary stimulation. Follicle-stimulating hormone
, T, and TSH all significantly maintained testis weight as compared wi
th Hx controls, although FSH and T, singly or in combination, were the
most effective. Contamination of the TSH preparation with trace amoun
ts of FSH was apparently responsible for the slight maintenance of tes
tis weight. A novel assay for determination of the numbers of viable g
erm cells was used in a subset of these groups to determine the cellul
ar sites of FSH and T action. Numbers of type A spermatogonia were low
ered after Hx and were maintained by either FSH or T or a combination
of these hormones. Other phases of germ-cell development most suscepti
ble to FSH and/or T were the successive conversions of type A spermato
gonia to intermediate spermatogonia, intermediate spermatogonia to typ
e B spermatogonia, preleptotene spermatocytes to pachytene spermatocyt
es, and early pachytene spermatocytes to intermediate maturity pachyte
ne spermatocytes during early and midcycle phases of pachytene spermat
ocyte development. Germ-cell loss during meiosis and virtually every p
hase of spermatid development was largely prevented by FSH or T or a c
ombination of these hormones. Thus, in testes in advanced stages of re
gression, both FSH and T were capable of preventing cell loss, suggest
ing that both hormones can affect the survival of the same cell type.
The present study demonstrated that FSH can partially compensate for l
owered T levels, The combined administration of FSH and T was more eff
ective in preventing overall cell degeneration than either hormone alo
ne. Unlike the initial phase of spermatogenesis, in which there is a l
argely midcycle loss of germ cells due to Hx, the loss of cells during
testis regression is more widespread and impacts several cell types i
n more than one stage of the spermatogenic cycle.