Maternal nicotine exposure and fetal programming of vascular oxidative stress in adult offspring

Research output: Contribution to journalLetterOther

12 Citations (Scopus)

Abstract

Despite the well-known harmful effects, many women continue to smoke throughout pregnancy. Consequently, nicotine replacement therapy (NRT) - which has been developed as a pharmacotherapy for smoking cessation - has been used as an alternative to smoking during pregnancy. However, like cigarette smoking, NRT results in biologically significant levels of nicotine crossing the placenta, leading to both fetal and neonatal exposure to nicotine, and yet, NRT safety during pregnancy has not been extensively evaluated. There is now evidence from studies in rats that maternal nicotine exposure throughout gestation results in fetal programming of vascular oxidative stress in the offspring during adulthood. This phenomenon involves vascular dysfunction mediated by reactive oxygen species in association with decreased superoxide dismutase activity and increased Nox2-NADPH oxidase expression in the vascular wall. If this phenomenon also occurs in humans, either smoking or NRT use during pregnancy may represent a novel risk factor for the unborn that results in accelerated cardiovascular disease in their adulthood. LINKED ARTICLE This article is a commentary on Xiao et al., pp. 1400-1409 of this issue. To view this paper visit http://dx.doi.org/10.1111/j.1476-5381.2011.01437.x.
Original languageEnglish
Pages (from-to)1397 - 1399
Number of pages3
JournalBritish Journal of Pharmacology
Volume164
Issue number5
DOIs
Publication statusPublished - 2011

Cite this

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title = "Maternal nicotine exposure and fetal programming of vascular oxidative stress in adult offspring",
abstract = "Despite the well-known harmful effects, many women continue to smoke throughout pregnancy. Consequently, nicotine replacement therapy (NRT) - which has been developed as a pharmacotherapy for smoking cessation - has been used as an alternative to smoking during pregnancy. However, like cigarette smoking, NRT results in biologically significant levels of nicotine crossing the placenta, leading to both fetal and neonatal exposure to nicotine, and yet, NRT safety during pregnancy has not been extensively evaluated. There is now evidence from studies in rats that maternal nicotine exposure throughout gestation results in fetal programming of vascular oxidative stress in the offspring during adulthood. This phenomenon involves vascular dysfunction mediated by reactive oxygen species in association with decreased superoxide dismutase activity and increased Nox2-NADPH oxidase expression in the vascular wall. If this phenomenon also occurs in humans, either smoking or NRT use during pregnancy may represent a novel risk factor for the unborn that results in accelerated cardiovascular disease in their adulthood. LINKED ARTICLE This article is a commentary on Xiao et al., pp. 1400-1409 of this issue. To view this paper visit http://dx.doi.org/10.1111/j.1476-5381.2011.01437.x.",
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Maternal nicotine exposure and fetal programming of vascular oxidative stress in adult offspring. / Lim, Rebecca; Sobey, Christopher.

In: British Journal of Pharmacology, Vol. 164, No. 5, 2011, p. 1397 - 1399.

Research output: Contribution to journalLetterOther

TY - JOUR

T1 - Maternal nicotine exposure and fetal programming of vascular oxidative stress in adult offspring

AU - Lim, Rebecca

AU - Sobey, Christopher

PY - 2011

Y1 - 2011

N2 - Despite the well-known harmful effects, many women continue to smoke throughout pregnancy. Consequently, nicotine replacement therapy (NRT) - which has been developed as a pharmacotherapy for smoking cessation - has been used as an alternative to smoking during pregnancy. However, like cigarette smoking, NRT results in biologically significant levels of nicotine crossing the placenta, leading to both fetal and neonatal exposure to nicotine, and yet, NRT safety during pregnancy has not been extensively evaluated. There is now evidence from studies in rats that maternal nicotine exposure throughout gestation results in fetal programming of vascular oxidative stress in the offspring during adulthood. This phenomenon involves vascular dysfunction mediated by reactive oxygen species in association with decreased superoxide dismutase activity and increased Nox2-NADPH oxidase expression in the vascular wall. If this phenomenon also occurs in humans, either smoking or NRT use during pregnancy may represent a novel risk factor for the unborn that results in accelerated cardiovascular disease in their adulthood. LINKED ARTICLE This article is a commentary on Xiao et al., pp. 1400-1409 of this issue. To view this paper visit http://dx.doi.org/10.1111/j.1476-5381.2011.01437.x.

AB - Despite the well-known harmful effects, many women continue to smoke throughout pregnancy. Consequently, nicotine replacement therapy (NRT) - which has been developed as a pharmacotherapy for smoking cessation - has been used as an alternative to smoking during pregnancy. However, like cigarette smoking, NRT results in biologically significant levels of nicotine crossing the placenta, leading to both fetal and neonatal exposure to nicotine, and yet, NRT safety during pregnancy has not been extensively evaluated. There is now evidence from studies in rats that maternal nicotine exposure throughout gestation results in fetal programming of vascular oxidative stress in the offspring during adulthood. This phenomenon involves vascular dysfunction mediated by reactive oxygen species in association with decreased superoxide dismutase activity and increased Nox2-NADPH oxidase expression in the vascular wall. If this phenomenon also occurs in humans, either smoking or NRT use during pregnancy may represent a novel risk factor for the unborn that results in accelerated cardiovascular disease in their adulthood. LINKED ARTICLE This article is a commentary on Xiao et al., pp. 1400-1409 of this issue. To view this paper visit http://dx.doi.org/10.1111/j.1476-5381.2011.01437.x.

UR - http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=21585345

U2 - 10.1111/j.1476-5381.2011.01488.x

DO - 10.1111/j.1476-5381.2011.01488.x

M3 - Letter

VL - 164

SP - 1397

EP - 1399

JO - British Journal of Pharmacology

JF - British Journal of Pharmacology

SN - 1476-5381

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