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Volume 87, Issue 3, Pages 565-571 (March 2007)


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Abnormal progression through meiosis in men with nonobstructive azoospermia

Fei Sun, M.D., Ph.D.ab, Paul Turek, M.D.c, Calvin Greene, M.D.d, Evelyn Ko, B.Sc.b, Alfred Rademaker, Ph.D.e, Renée H. Martin, Ph.D.abCorresponding Author Informationemail address

Received 4 May 2006; received in revised form 24 July 2006; accepted 24 July 2006. published online 30 November 2006.

Objective

To study meiotic abnormalities in men with nonobstructive azoospermia.

Design

Analysis of synaptonemal complex and recombination in testicular tissue.

Setting

Research laboratory.

Patient(s)

Twenty-nine men with nonobstructive azoospermia and 12 men with normal spermatogenesis.

Intervention(s)

Testicular tissues were processed with immunofluorescent staining using antibodies against proteins associated with synaptonemal complex and recombination events.

Main Outcome Measure(s)

Synaptonemal complex configuration and recombination in meiosis I.

Result(s)

In patients with nonobstructive azoospermia, a marked heterogeneity in spermatogenesis was found: nearly half of them had a complete absence of meiotic cells, one case had germ cells arrested at the zygotene stage of meiotic prophase, and, in general, the rest had impaired fidelity of chromosome synapsis and recombination in pachytene cells. Compared with controls, these patients had significantly more cells in leptotene/zygotene and higher frequencies of unpaired chromosome regions in pachytene. Significantly reduced recombination, an increased frequency of achiasmate autosome bivalents, and sex univalents in pachytene were also observed in these patients with nonobstructive azoospermia.

Conclusion(s)

Defects in chromosome synapsis and decreased recombination during meiotic prophase may have led to spermatogenesis arrest and contributed in part to the unexplained infertility in these patients.

a Department of Medical Genetics, University of Calgary, Calgary, Alberta, Canada

b Department of Genetics, Alberta Children’s Hospital, Calgary, Alberta, Canada

c Department of Urology, Obstetrics and Gynecology and Reproductive Sciences, University of California, San Francisco, California

d Department of Obstetrics and Gynecology, University of Calgary, Calgary, Alberta, Canada

e Department of Preventive Medicine, Northwestern University Medical School, Chicago, Illinois

Corresponding Author InformationReprint requests: Renée H. Martin, Ph.D., Department of Genetics, Alberta Children’s Hospital, 1820 Richmond Road S.W., Calgary, Alberta, Canada T2T 5C7 (FAX: 403-543-9100).

 Supported by Canadian Institutes of Health Research grant (MA7961 to R.H.M.) and Canada Research Chair in Genetics (to R.H.M.).

PII: S0015-0282(06)04030-1

doi:10.1016/j.fertnstert.2006.07.1531


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