Use of fluorescence in situ hybridization (FISH) to assess effects of smoking, caffeine, and alcohol on aneuploidy load in sperm of healthy men

Robbins, Wendie A.; Vine, Marilyn F.; Truong, Kinh; Everson, Richard B.

doi:10.1002/(sici)1098-2280(1997)30:2<175::aid-em10>3.0.co;2-a

Cited by 139 publications

(85 citation statements)

References 42 publications

(2 reference statements)

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“…These procedures have been adapted from Robbins et al (5). We used a commercial kit (CEP X spectrum orange, Y spectrum green, and 18 spectrum aqua direct-labeled fluorescent DNA probes; Vysis, Inc., Downers Grove, IL, USA).…”

Section: Methodsmentioning

confidence: 99%

“…The majority of aneuploidy is believed to be due to nondisjunction during meiosis (4). It has been estimated that 4 of 1,000 live births and 35% of spontaneous abortions are aneuploid and that an important proportion of aneuploidy occurring in embryos and newborns are of paternal origin (5,6). Paternal contribution to these aneuploidies range from 10% to 100%, depending on the specific chromosome involved (7).…”

mentioning

confidence: 99%

“…In humans, age, lifestyle (alcohol intake and smoking), and chemotherapy can increase risks for sex-chromosome and autosomal aneuploidies (5,(8)(9)(10)(11)(12)(13). Exposure to organophosphorous pesticides (OP), used worldwide, has also been associated with hyperploidy/polyploidy in sperm (14,15) Aneuploidy is a common cause of poor reproductive outcomes in humans and is associated with severe medical problems in live newborns presenting genetic syndromes.…”

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confidence: 99%

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Organophosphorous Pesticide Exposure Increases the Frequency of Sperm Sex Null Aneuploidy

Recio¹,

Robbins²,

Ocampo-Gomez³

et al. 2001

Environmental Health Perspectives

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Organophosphorous Pesticide Exposure Increases the Frequency of Sperm Sex Null Aneuploidy

Recio¹,

Robbins²,

Ocampo-Gomez³

et al. 2001

Environmental Health Perspectives

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“…It has been well documented that severe male infer tility correlates with a significant increase in sperm aneuploidy; in addition, other factors such as paternal age, chemotherapy treatment, smoking and alcohol have also been associated with increased sperm aneuploidy [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16]. Given the significant increased risk of sperm aneuploidy in infertile men, concerns have been raised regarding whether these individuals are at a higher risk of giving rise to aneuploid pregnancies when treated by intracytoplasmic sperm injection (ICSI) [17].…”

Section: Introductionmentioning

confidence: 99%

Scoring of sperm chromosomal abnormalities by manual and automated approaches: qualitative and quantitative comparisons

Tempest¹,

Cheng²,

Gillott³

et al. 2009

Asian J Androl

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It is now well known that levels of sperm disomy correlate to levels of infertility (as well as other factors). The risk of perpetuating aneuploidy to the offspring of infertile males undergoing intracytoplasmic sperm injection (ICSI) has become a hotly debated issue in assisted reproduction; however, there remain barriers to the practical implementation of offering sperm disomy screening in a clinical setting. The major barrier is the operator time taken to analyze a statistically meaningful (sufficient) number of cells. The introduction of automated 'spot counting' software-hardware combinations presents a potential solution to this problem. In this preliminary validation study, we analyzed 10 patients, both manually and using a commercially available spot counter. Results show a statistically significant correlation between both approaches for scoring of sperm disomy, but no correlation is found when scoring for diploid sperm. The most likely explanation for the latter is an apparent overscoring of two closely associated sperm heads as a single diploid cell. These results, and similar further studies that will ensue, help to inform cost-benefit analyses that individual clinics need to carry out in order to decide whether to adopt sperm aneuploidy screening as a routine tool for the assessment of sperm from men requiring ICSI treatment.

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“…Indeed, several studies have reported elevated levels of DNA base damage [61], DNA adducts [62,63] and DNA strand breaks [64] in sperm of smokers. Studies using FISH have also shown that smokers have increased levels of chromosomal defects in their sperm [65][66][67]. It is tempting to speculate that daily tobacco smoke may induce accumulation of DNA damage in sperm especially during the last two or three weeks before fertilization and that even moderate smoking may lead to accumulated detrimental effects on the genetic integrity of the fertilizing sperm.…”

Section: Discussionmentioning

confidence: 99%

DNA Repair Decline During Mouse Spermiogenesis Results in the Accumulation of Heritable DNA Damage

Marchetti¹,

Wyrobek²

2007

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The post-meiotic phase of mouse spermatogenesis (spermiogenesis) is very sensitive to the genomic effects of environmental mutagens because as male germ cells form mature sperm they progressively lose the ability to repair DNA damage. We hypothesized that repeated exposures to mutagens during this repair-deficient phase result in the accumulation of heritable genomic damage in mouse sperm that leads to chromosomal aberrations in zygotes after fertilization. We used a combination of single or fractionated exposures to diepoxybutane (DEB), a component of tobacco smoke, to investigate how differential DNA repair efficiencies during the three weeks of spermiogenesis affected the accumulation of DEB-induced heritable damage in early spermatids (21-15 days before fertilization, dbf), late spermatids (14-8 dbf) and sperm (7-1 dbf). Analysis of chromosomal aberrations in zygotic metaphases using PAINT/DAPI showed that late spermatids and sperm are unable to repair DEB-induced DNA damage as demonstrated by significant increases (P<0.001) in the frequencies of zygotes with chromosomal aberrations. Comparisons between single and fractionated exposures suggested that the DNA repair-deficient window during late spermiogenesis may be less than two weeks in the mouse and that during this repair-deficient window there is accumulation of DNA damage in sperm.Finally, the dose-response study in sperm indicated a linear response for both single and repeated exposures. These findings show that the differential DNA repair capacity of post-meioitic male germ cells has a major impact on the risk of paternally transmitted heritable damage and suggest that chronic exposures that may occur in the weeks prior to fertilization because of occupational or lifestyle factors (i.e, smoking) can lead to an accumulation of genetic damage in sperm and result in heritable chromosomal aberrations of paternal origin.

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Use of fluorescence in situ hybridization (FISH) to assess effects of smoking, caffeine, and alcohol on aneuploidy load in sperm of healthy men

Cited by 139 publications

References 42 publications

Organophosphorous Pesticide Exposure Increases the Frequency of Sperm Sex Null Aneuploidy

Organophosphorous Pesticide Exposure Increases the Frequency of Sperm Sex Null Aneuploidy

Scoring of sperm chromosomal abnormalities by manual and automated approaches: qualitative and quantitative comparisons

DNA Repair Decline During Mouse Spermiogenesis Results in the Accumulation of Heritable DNA Damage

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