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* To whom correspondence should be addressed. E-mail: mark.hedger{at}med.monash.edu.au.
Male fertility is inhibited by inflammatory disease, but the mechanisms responsible are poorly defined. The effects of acute systemic inflammation induced by a single i.p. injection of lipopolysaccharide (LPS) on spermatogenic function in adult male rats was investigated using detailed stereological analysis. The earliest effect observed was a significant maturational delay of meiosis during the leptotene/zygotene phase (at stages IX-XIII) within 24 h. This was followed within six days by an increase in premature release of these cells and the adjacent, more lumenally located generation of round spermatids from the seminiferous epithelium. An increase in germ cell apoptosis within stages IX-XIII also occurred at this time. These data indicate that the initial effects of acute inflammation on the seminiferous epithelium are most pronounced on stages IX-XIII. The effects were not consistent with a loss of hormonal regulation, suggesting that a direct effect of inflammation on the function of the Sertoli cell during this critical stage of meiosis is involved. In the longer term, however, the consequences of this acute inflammatory episode were relatively minor: within 28 days there had been a compensatory increase in the efficiency of the seminiferous epithelium, restoring the spermatogenic capacity of the testis towards pre-inflammation levels.
Key words: Androgen
Fertility
Hormone
Infertility
Testis
Sertoli cell
apoptosis
inflammation
meiosis
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