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Published-Ahead-of-Print September 20, 2006, DOI:10.2164/jandrol.106.000752
Journal of Andrology, Vol. 28, No. 1, January/February 2007
Copyright © American Society of Andrology
DOI: 10.2164/jandrol.106.000752

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A Stereological Analysis of the Response of Spermatogenesis to an Acute Inflammatory Episode in Adult Rats

SENG H. LIEW*,{dagger}, SARAH J. MEACHEM{dagger} AND MARK P. HEDGER*

From the * Monash Institute of Medical Research, Monash University, and {dagger} Prince Henry's Institute of Medical Research, Monash Medical Centre, Melbourne, Australia.

Correspondence to: A/Prof Mark Hedger, Monash Institute of Medical Research, Monash University, 27-31 Wright Street, Clayton, Victoria 3168, Australia (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 IP injection of lipopolysaccharide (LPS) on spermatogenic function in adult male rats were 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 hours. This was followed within 6 days by an increase in premature release of these cells and the adjacent, more luminally 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 preinflammation levels.

     Key words: Apoptosis, meiosis, Sertoli cell, inflammation, fertility




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