Smoking during pregnancy causes double-strand DNA break damage to the placenta

Slatter, Tania L.; Park, Lydia; Anderson, Karyn; Lailai-Tasmania, Viwa; Herbison, Peter; Clow, W. M.; Royds, Janice A.; Devenish, Celia; Hung, Noelyn

doi:10.1016/j.humpath.2013.07.024

Cited by 21 publications

(17 citation statements)

References 32 publications

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“…There are several studies on the link between smoking and γ-H2AX formation [7]–[10]. Most of those studies are in vitro experiments showing that cigarette smoke induces γ-H2AX formation in cultured cells.…”

Section: Discussionmentioning

confidence: 99%

“…Most of those studies are in vitro experiments showing that cigarette smoke induces γ-H2AX formation in cultured cells. There is one human study that observed a marked increase in γ-H2AX-positive cells in the placentae from smokers [10]. However, none of these studies showed reversibility of the DSBs in response to smoking cessation within individual subjects.…”

Section: Discussionmentioning

confidence: 99%

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Smoking Cessation Reverses DNA Double-Strand Breaks in Human Mononuclear Cells

Ishida

Tashiro

et al. 2014

PLoS ONE

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ObjectiveCigarette smoking is a major risk factor for atherosclerotic cardiovascular disease, which is responsible for a significant proportion of smoking-related deaths. However, the precise mechanism whereby smoking induces this pathology has not been fully delineated. Based on observation of DNA double-strand breaks (DSBs), the most harmful type of DNA damage, in atherosclerotic lesions, we hypothesized that there is a direct association between smoking and DSBs. The goal of this study was to investigate whether smoking induces DSBs and smoking cessation reverses DSBs in vivo through examination of peripheral mononuclear cells (MNCs).Approach and ResultsImmunoreactivity of oxidative modification of DNA and DSBs were increased in human atherosclerotic lesions but not in the adjacent normal area. DSBs in human MNCs isolated from the blood of volunteers can be detected as cytologically visible “foci” using an antibody against the phosphorylated form of the histone H2AX (γ-H2AX). Young healthy active smokers (n = 15) showed increased γ-H2AX foci number when compared with non-smokers (n = 12) (foci number/cell: median, 0.37/cell; interquartile range [IQR], 0.31–0.58 vs. 4.36/cell; IQR, 3.09–7.39, p<0.0001). Smoking cessation for 1 month reduced the γ-H2AX foci number (median, 4.44/cell; IQR, 4.36–5.24 to 0.28/cell; IQR, 0.12–0.53, p<0.05). A positive correlation was noted between γ-H2AX foci number and exhaled carbon monoxide levels (r = 0.75, p<0.01).ConclusionsSmoking induces DSBs in human MNCs in vivo, and importantly, smoking cessation for 1 month resulted in a decrease in DSBs to a level comparable to that seen in non-smokers. These data reinforce the notion that the cigarette smoking induces DSBs and highlight the importance of smoking cessation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Smoking Cessation Reverses DNA Double-Strand Breaks in Human Mononuclear Cells

Ishida

Tashiro

et al. 2014

PLoS ONE

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“…Any further histopathological abnormalities, such as necrotizing deciduitis, were descriptively recorded. Smoking history was correlated with the DNA-damage pattern in the placenta, 23 to ensure that there was minimal effect of undeclared smoking on measured complications.…”

Section: Methodsmentioning

confidence: 99%

“…We obtained singleton placentae (n = 339) from the Otago Placenta Study, which comprises 720 placentae collected during 2009-2014 [23]. Parent/s provided signed informed consent and ethical approval was obtained from the New Zealand Health and Disabilities Multiregional Ethics and Lower Regional South Ethics Committees (LRS/09/09/038).…”

Section: Participantsmentioning

confidence: 99%

A clinicopathological study of episomal papillomavirus infection of the human placenta and pregnancy complications

et al. 2015

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Viral infections are known to adversely affect pregnancy, but scant attention has been given to human papilloma virus (HPV) infection. We aimed to determine the molecular and histopathological features of placental HPV infection, in association with pregnancy complications including fetal growth restriction, pre-maturity, pre-eclampsia, and diabetes. Three hundred and thirty-nine placentae were selected based on the presence or absence of pregnancy complications. Five independent methods were used to identify HPV in the placenta, namely, immunohistochemistry for L1 viral capsid, in situ hybridization to high-risk HPV DNA, PCR, western blotting, and transmission electron microscopy. Pregnancy complications and uterine cervical smear screening results were correlated with placental HPV histopathology. In this study, which was deliberately biased towards complications, HPV was found in the decidua of 75% of placentae (253/339) and was statistically associated with histological acute chorioamnionitis (P o0.05). In 14% (35/253) of the HPV positive cases, HPV L1 immunoreactivity also occurred in the villous trophoblast where it was associated with a lymphohistiocytic villitis (HPV-LHV), and was exclusively of high-risk HPV type. HPV-LHV significantly associated with fetal growth restriction, preterm delivery, and pre-eclampsia (all P o0.05). All cases of pre-eclampsia (20/20) in our cohort had high-risk placental HPV. A further 55 cases (22%, 55/253) of HPV positive placentae had minimal villous trophoblast HPV L1 immunoreactivity, but a sclerosing pauci-immune villitis, statistically associated with diabetes (49.1%, 27/55, Po 0.05). For women with placental HPV, 33% (69/207) had an HPV-related positive smear result before pregnancy compared with (9.4% 8/85) of women with HPV-negative placentae (P = 0.0001). Our findings support further investigations to determine if vaccination of women and men will improve pregnancy outcomes. Modern Pathology (2015Pathology ( ) 28, 1369Pathology ( -1382 doi:10.1038/modpathol.2015 published online 21 August 2015 In the immune and hormonal modulated milieu of pregnancy, viruses are well known to infect the placenta, developing fetus, and neonate. The most common and important neoplastic driver of the lower uterine tract, human papillomavirus (HPV), 1 has been detected in the uterine cervix of 15-25% of pregnant women 2-6 and a cervical HPV infection during pregnancy has been associated with a higher incidence of spontaneous abortions, 7-9 premature rupture of the membranes, 10 spontaneous preterm labor, 11,12 pre-eclampsia, 13 and placental 'villitis' not otherwise specified. 12 HPV DNA has been detected in the placenta and amniotic fluid. 7,11,[14][15][16][17]11,16,18,and 31 have been shown to replicate in trophoblast cell lines, [18][19][20] where HPV infection decreased trophoblast number and trophoblast-endometrial cell adhesion in vitro. 19,20 We investigated for the presence of HPV in the placenta and carried out a histopathological and molecular cross-sectional study of 339 ...

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“…29 This discovery may provide an explanation for how intrauterine exposures can influence the development of the fetus, cause fetal telomere shortening, and inevitably lead to adult disease.…”

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confidence: 99%

Telomere length and fetal programming: A review of recent scientific advances

Whiteman¹,

Goswami²,

Salihu

2017

American J Rep Immunol

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We sought to synthesize a comprehensive literature review comprising recent research linking fetal programming to fetal telomere length. We also explored the potential effects fetal telomere length shortening has on fetal phenotypes. Utilizing the PubMed database as our primary search engine, we retrieved and reviewed 165 articles of published research. The inclusion criteria limited the articles to those that appeared within the last ten years, were pertinent to humans, and without restriction to language of publication. Our results showed that socio-demographic factors like age, sex, genetic inheritance, and acquired disease impact telomere length. Further, we found several maternal characteristics to be associated with fetal telomere length shortening, and these include maternal chemical exposure (eg, tobacco smoke), maternal stress during pregnancy, maternal nutritional and sleeping disorders during pregnancy as well as maternal disease status. Due to paucity of data, our review could not synthesize evidence directly linking fetal phenotypes to telomere length shortening.Although the research summarized in this review shows some association between determinants of intrauterine programming and fetal telomere length, there is still significant work that needs to be done to delineate the direct relationship of telomere attrition with specific fetal phenotypes. K E Y W O R D Sfetal phenotypes, fetal programming, telomere length

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Smoking during pregnancy causes double-strand DNA break damage to the placenta

Cited by 21 publications

References 32 publications

Smoking Cessation Reverses DNA Double-Strand Breaks in Human Mononuclear Cells

Smoking Cessation Reverses DNA Double-Strand Breaks in Human Mononuclear Cells

A clinicopathological study of episomal papillomavirus infection of the human placenta and pregnancy complications

Telomere length and fetal programming: A review of recent scientific advances

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