Chromosomal Instability in Amniocytes From Fetuses of Mothers Who Smoke

Chica, Rosa Ana de la; Ribas, Isabel; Giraldo, Jesús; Egozcue, J.; Fuster, Carme

doi:10.1001/jama.293.10.1212

Cited by 79 publications

(37 citation statements)

References 28 publications

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“…The results showed increased DNA damage levels in neonates with antenatal ETS exposure. These results are consistent with the results found by examining SCE or frequency of chromosomal aberrations (21,35,36).…”

Section: Discussionsupporting

confidence: 92%

“…A study of white population showed that there is an increased susceptibility to DNA damage from PAHs and the diminished ability to clear ETS components for the fetus (20). de la Chica et al found that maternal smoking exposure increase structural chromosomal abnormalities and chromosomal lesions in fetus (21). However, the effect of genotoxicity determined by comet assay for infants with prenatal smoking exposure has not been well documented.…”

mentioning

confidence: 99%

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Prenatal Smoking Exposure and Neonatal DNA Damage in Relation to Birth Outcomes

Tsui

Lin

et al. 2008

Pediatr Res

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This study investigated whether mothers with prenatal environmental tobacco smoke (ETS) exposure increased the newborn genetic damage and adverse birth outcomes. Study participants were women receiving prenatal care at three hospitals in Central Taiwan and their newborns. Participants were divided into two groups (nonsmokers and ETS-exposed non-smokers) based on maternal ETSexposed status. Comet assay were performed for cord blood samples. Infants born to mothers with prenatal ETS exposure had the highest mean cord blood DNA damage score (69.7 Ϯ 42.3) and poorer birth outcomes. No negative fetal growth effects appeared among newborns with low DNA damage levels. Among newborns with high DNA damage levels (comet scores Ͼ50), those born to prenatal ETS exposure had an average reduction of 252.7 g in birth weight, 1.10 cm shorter in length and a 0.92-cm decrease in head circumference, compared to newborns with no smoking exposure. This study shows that the DNA damage scores can be used as an effect-modifier on the relationships between ETS exposure and adverse birth outcome. The association appears more apparent for the ETS exposure in relation with more severe DNA damage. S tudies have suggested adverse reproductive outcomes among newborns in relation to maternal cigarette smoking and environmental tobacco smoke (ETS) exposure during pregnancy. Most of these studies are based on self-reported smoking status, and serum or urinary cotinine levels as the exposure measures (1-6). Some studies failed to find a significant association (7-11). The discrepancy could be explained by the variability of study populations, sample size, study design, and individual susceptibility (12,13). Other markers linking the association between smoking and/or ETS and pregnant outcomes deserve exploration.Cigarette smoke contains more than 4000 chemicals (14), including carcinogens such as polycyclic aromatic hydrocarbons (PAHs), arylmines, N-nitrosamines (15,16), and aromatic amines. These compounds can cross the placenta and experimental animal studies have indicated that the fetus and newborn are more susceptible to carcinogens than adults (17)(18)(19). A study of white population showed that there is an increased susceptibility to DNA damage from PAHs and the diminished ability to clear ETS components for the fetus (20). de la Chica et al. found that maternal smoking exposure increase structural chromosomal abnormalities and chromosomal lesions in fetus (21). However, the effect of genotoxicity determined by comet assay for infants with prenatal smoking exposure has not been well documented. The comet assay is a sensitive technique allowing the detection of DNA damage at the single cell level. This assay is also effective in detecting DNA damage induced by tobacco smoke toxicants in white blood cells (22).The smoking prevalence among women in Taiwan has recently increased to 5.95%, and as many as 42.4% of women are daily exposed to ETS (23). Another studies in Taiwan showed that 58% of pregnant women and 57% of neversmoked wo...

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

Prenatal Smoking Exposure and Neonatal DNA Damage in Relation to Birth Outcomes

Tsui

Lin

et al. 2008

Pediatr Res

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“…In addition, there is also a case report of leukemia with t(4;11)(q21;q23) following exposure to benzol [169]. Finally, cigarette smoke is an environmental source of benzene, smoking during pregnancy is associated with chromosomal instability in fetal amniocytes, and the genomic region most affected by tobacco is 11q23 [170].…”

Section: Covalent Topoisomerase II Poisonsmentioning

confidence: 99%

DNA topoisomerase II, genotoxicity, and cancer

McClendon

Osheroff

2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

363

466

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Type II topoisomerases are ubiquitous enzymes that play essential roles in a number of fundamental DNA processes. They regulate DNA under-and overwinding, and resolve knots and tangles in the genetic material by passing an intact double helix through a transient double-stranded break that they generate in a separate segment of DNA. Because type II topoisomerases generate DNA strand breaks as a requisite intermediate in their catalytic cycle, they have the potential to fragment the genome every time they function. Thus, while these enzymes are essential to the survival of proliferating cells, they also have significant genotoxic effects. This latter aspect of type II topoisomerase has been exploited for the development of several classes of anticancer drugs that are widely employed for the clinical treatment of human malignancies. However, considerable evidence indicates that these enzymes also trigger specific leukemic chromosomal translocations. In light of the impact, both positive and negative, of type II topoisomerases on human cells, it is important to understand how these enzymes function and how their actions can destablize the genome. This article discusses both aspects of human type II topoisomerases.

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“…A recent study on fetal chromosomes and maternal smoking concluded that smoking during pregnancy induces chromosomal instability. 16 Most lung cancer patients are smokers, and in populations with long-term cigarette use, the population-attributable risk of smoking is thought to be up to 90%. 5 Probably only prospective data on smoking can reach higher levels of accuracy.…”

Section: Discussionmentioning

confidence: 99%

“…For the excesses of bladder and kidney cancers, we propose a contribution of tobacco carcinogens that are transmitted through breastfeeding and in utero exposure. We admit that our inferences are based on indirect data, but we wish that they encourage more direct approaches, such as the recent chromosomal studies, 16 to address these questions of tobacco carcinogenesis with implications to the health of the offspring. …”

Section: Discussionmentioning

confidence: 99%

Parental lung cancer as predictor of cancer risks in offspring: Clues about multiple routes of harmful influence?

Hemminki

Chen

2005

Intl Journal of Cancer

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The carcinogenic effects of active smoking have been demonstrated for many sites, but the effects of passive smoking and exposures during pregnancy and breastfeeding are less well documented. We examined whether 0–70‐year‐old offspring of parents with lung cancer are at a risk of cancer that cannot be explained by their smoking or familial risk. It was assumed that known target sites for tobacco carcinogenesis would be affected, if any. The nationwide Swedish Family‐Cancer Database with cancers recorded from 1958 to 2002 was used to calculate age‐specific standardized incidence ratios (SIRs). Among offspring of affected mothers, increased risks were observed for upper aerodigestive (SIR 1.45), nasal (2.93), lung (1.71) and bladder (1.52) cancers and for kidney cancer (6.41) in one age group. The risk of bladder cancer was found in younger age groups than that of lung cancer. Cancers at many of these sites, but not the kidney or the bladder, were in excess in offspring of affected fathers. Nasal cancer was even increased when either parent was diagnosed with lung cancer; the highest risk was for nasal adenoid cystic carcinoma (7.73). The data suggest that passive smoking during childhood is associated with an increase risk of nasal cancer. For bladder and kidney cancers, a contribution by tobacco carcinogens is implicated through breastfeeding and in utero exposure. © 2005 Wiley‐Liss, Inc.

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Chromosomal Instability in Amniocytes From Fetuses of Mothers Who Smoke

Cited by 79 publications

References 28 publications

Prenatal Smoking Exposure and Neonatal DNA Damage in Relation to Birth Outcomes

Prenatal Smoking Exposure and Neonatal DNA Damage in Relation to Birth Outcomes

DNA topoisomerase II, genotoxicity, and cancer

Parental lung cancer as predictor of cancer risks in offspring: Clues about multiple routes of harmful influence?

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