Cytogenetics and infertility in man*: II. Testicular histology and meiosis

Chandley, Ann C.; MacLean, Nancy; Edmond, P.; Fletcher, J.; Watson, G. Stennis

doi:10.1111/j.1469-1809.1976.tb00176.x

Cited by 85 publications

(45 citation statements)

References 28 publications

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“…Chandley et al [23] showed a reduced proportion of spermatids and spermatozoa on testicular biopsy in subfertile balanced translocations carriers. Balanced, structural chromosome aberrations seldom result in azoospermia [20,24].…”

Section: Discussionmentioning

confidence: 99%

Sperm parameters and DNA fragmentation of balanced chromosomal rearrangements carriers

Pastuszek¹,

Kiewisz²,

Kulwikowska³

et al. 2016

Folia Histochem Cytobiol.

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Introduction. Somatic chromosomal rearrangements that occur in infertile males are thought to be one of the major genetic factors influencing male infertility. The objective of this retrospective study was to evaluate sperm parameters in a group of patients with balanced translocations. Material and methods. We analyzed semen of 84 balanced somatic translocation carriers [35 Robertsonian translocation (RT group) and 49 reciprocal translocation (RCT group)] and 57 men with normal karyotype (control group). Semen samples were evaluated for sperm concentration, its motion parameters and vitality, round cell number (CASA) and DNA fragmentation index (TUNEL). Cytogenetic evaluation was also performed for each study participant. Results. Sperm concentrations were lower when comparing the RT group to the control (p < 0.001) and RCT groups (p < 0.05). Occurrence of abnormal sperm concentration was more common among RT carriers (74.3%) than in the other groups (42.9% in RCT group and 28.1% in control group). The sperm progressive motility and vitality in RT carriers (21.53% and 62.17%) were lower than in control group (39.77% and 77.47%, p < 0.001, respectively) and RCT carriers (31.47% and 76.17%, p < 0.001, respectively). The RCT carriers and the control group did not differ in regard to sperm concentration, progressive sperm motility, motility grade D and sperm vitality. There were no significant differences in DNA fragmentation in carriers of both studied structural chromosomal rearrangements in comparison to subjects with normal karyotype. Conclusions. RT carriers had significantly lower semen parameters in comparison to not only the subjects with normal karyotypes but also the RCT carriers.

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Section: Discussionmentioning

confidence: 99%

Sperm parameters and DNA fragmentation of balanced chromosomal rearrangements carriers

Pastuszek¹,

Kiewisz²,

Kulwikowska³

et al. 2016

Folia Histochem Cytobiol.

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“…Thus, histone deacetylation seems to play a key role in preventing aneuploidy during female meiosis. In somatic cells and mammalian male germ cells, a spindle assembly checkpoint monitors chromosome alignment and spindle integrity during cell division (19,20). In the absence of proper chromosome alignment, the cell cycle is arrested or anaphase is delayed, allowing the cell to correct errors that might otherwise produce aneuploid progeny.…”

Section: Discussionmentioning

confidence: 99%

Inadequate histone deacetylation during oocyte meiosis causes aneuploidy and embryo death in mice

Akiyama

Nagata

Aoki

2006

Proc. Natl. Acad. Sci. U.S.A.

163

130

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Errors in meiotic chromosome segregation are the leading cause of spontaneous abortions and birth defects. Almost all such aneuploidy derives from meiotic errors in females, with increasing maternal age representing a major risk factor. It was recently reported that histones are globally deacetylated in mammalian oocytes during meiosis but not mitosis. In the present study, inhibition of meiotic histone deacetylation was found to induce aneuploidy in fertilized mouse oocytes, which resulted in embryonic death in utero at an early stage of development. In addition, a histone remained acetylated in the oocytes of older (10-monthold) female mice, suggesting that the function for histone deacetylation is decreased in the oocytes of such mice. Thus, histone deacetylation may be involved in the fair distribution of chromosomes during meiotic division. The high incidence of aneuploidy in the embryos of older females may be due to inadequate meiotic histone deacetylation.acetylation ͉ meiotic maturation ͉ chromosome segregation

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“…Studies at these meiotic stages are scarce, owing to the difficulty of obtaining testicular tissue. Meiotic analyses carried out on fertile and infertile men described abnormal chiasma count and numerical chromosome abnormalities (Skakkebaek et al, 1973;Chandley et al, 1976;Koulischer et al, 1982;Egozcue et al, 1983;Laurie et al, 1985;Guichaoua et al, 1986;Uroz et al, 2009Uroz et al, , 2011 but they were not focused on studying non-disjunction mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Meiotic non-disjunction mechanisms in human fertile males

Uroz

Templado

2012

Human Reproduction

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background: In humans, little is known about the mechanisms of non-disjunction working in male meiosis, although considerable attention has been given to these mechanisms in female meiosis. The present study explores the origin of meiotic non-disjunction during human spermatogenesis and the chromosomes most commonly involved in this process. methods:We used Multiplex fluorescence in situ hybridization to carry out meiotic analyses in metaphase I (MI) and metaphase II (MII) spermatocytes from three fertile donors. Testicular biopsy was obtained during a vasectomy procedure.results: We examined a total of 317 MI and 248 MII spermatocytes. The frequency of numerical chromosome abnormalities at MII (14.5%) was 5.5 times higher than at MI (2.5%). We observed 88 (27.7%) spermatocytes I with chromosome bivalents with a low chiasma count, usually small chromosomes displaying two separated univalents. Chromosomes X, Y and 21 were the most commonly found as achiasmate chromosomes at MI and the most frequently involved in disomy at MII. Hyperploidy frequency in spermatocytes II (disomy) was significantly higher (P , 0.001) than that found in spermatocytes I (trisomy).conclusions: Achiasmate non-disjunction and premature separation of sister chromatids appear to be the two main non-disjunction mechanisms during the first meiotic division in human spermatogenesis, and both mechanisms contribute equally to the genesis of aneuploidy. The elevated frequencies of disomy detected in spermatocytes II are significantly higher than those previously described in human spermatozoa, suggesting the existence of a postmeiotic checkpoint monitoring numerical abnormalities.

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Cytogenetics and infertility in man*: II. Testicular histology and meiosis

Cited by 85 publications

References 28 publications

Sperm parameters and DNA fragmentation of balanced chromosomal rearrangements carriers

Sperm parameters and DNA fragmentation of balanced chromosomal rearrangements carriers

Inadequate histone deacetylation during oocyte meiosis causes aneuploidy and embryo death in mice

Meiotic non-disjunction mechanisms in human fertile males

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