Maternal cigarette smoking increases F2-isoprostanes and reduces prostacyclin and nitric oxide in umbilical vessels

Obwegeser, R.; Oguogho, A.; Ulm, Martin; Berghammer, Peter; Sinzinger, H.

doi:10.1016/s0090-6980(99)00011-8

Cited by 44 publications

(27 citation statements)

References 20 publications

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“…33,34 Apparently, the present reduction in eNOS activity associated with smoking in pregnancy was not mediated by changes in plasma levels of estradiol, 35 ADMA, and the eNOS substrate L-arginine. 36 Figure. eNOS activity (A) and eNOS concentration (B) in fetal ECs from umbilical veins of maternal nonsmokers (nϭ182), smokers (nϭ43), and ex-smokers (nϭ41).…”

Section: Discussionmentioning

confidence: 99%

Smoking Cessation Early in Pregnancy and Birth Weight, Length, Head Circumference, and Endothelial Nitric Oxide Synthase Activity in Umbilical and Chorionic Vessels

Andersen

Simonsen²,

Uldbjerg³

et al. 2009

Circulation

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Background-Reduced production of the vasodilator nitric oxide (NO) in fetal vessels in pregnant smokers may lower the blood flow to the fetus and result in lower birth weight, length, and head circumference. The present study measured endothelial NO synthase (eNOS) activity in fetal umbilical and chorionic vessels from nonsmokers, smokers, and ex-smokers and related the findings to the fetal outcome. Methods and Results-Of 266 healthy, singleton pregnancies, 182 women were nonsmokers, 43 were smokers, and 41 stopped smoking early in pregnancy. eNOS activity and concentration were quantified in endothelial cells of the fetal vessels. Cotinine, lipid profiles, estradiol, L-arginine, and dimethylarginines that may affect NO production were determined in maternal and fetal blood. Serum cotinine verified self-reported smoking. Newborns of smokers had a lower weight (PՅ0.001) and a smaller head circumference (PՅ0.041) and were shorter (PՅ0.001) than newborns of nonsmokers and ex-smokers. eNOS activity in umbilical veins of smokers was 36% lower (PϽ0.001), eNOS concentration was 47% lower (PϽ0.001), and the fetal plasma level of high-density lipoprotein was 18% lower (PϽ0.001) than those of nonsmokers, whereas the same levels were found in umbilical veins from ex-smokers and nonsmokers. The same patterns in eNOS activity and concentration were found in umbilical arteries and chorionic vessels. Fetal plasma levels of estradiol, L-arginine, dimethylarginines, total cholesterol, and triglycerides were similar for nonsmokers, smokers, and ex-smokers. Conclusions-The findings suggest that maternal smoking reduces eNOS activity in the fetal vascular bed, contributing to retarded fetal growth caused by the reduction of vasodilatory capacity, and suggest that smoking cessation early in pregnancy prevents these effects in newborns. (Circulation. 2009;119:857-864.)

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Section: Discussionmentioning

confidence: 99%

Smoking Cessation Early in Pregnancy and Birth Weight, Length, Head Circumference, and Endothelial Nitric Oxide Synthase Activity in Umbilical and Chorionic Vessels

Andersen

Simonsen²,

Uldbjerg³

et al. 2009

Circulation

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“…Studies directed at measuring F 2 -isoprostanes in vascular walls reveal the presence [65, 66]or absence [67]of measurable amount of F 2 -isoprostanes. They can be detected at birth in umbilical cords, where their concentration increases with maternal cigarette smoking [68]. In human atherosclerotic lesions (aorta, femoral, popliteal, anterior tibial and vertebral arteries), isoprostane concentrations (pg/mg dry weight) are increased 6.5-fold and the isoprostane/arachidonic acid ratio 4-fold compared to umbilical veins [65].…”

Section: Production Of Isoprostanes In the Vascular Wallmentioning

confidence: 99%

Vascular Biology of the Isoprostanes

Cracowski¹,

Devillier²,

Stanke‐Labesque³

et al. 2001

J Vasc Res

101

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Isoprostanes are a family of compounds produced from polyunsaturated fatty acids via a free-radical-catalysed mechanism. F₂-isoprostanes are prostaglandin F_2α isomers derived from arachidonic acid. These compounds induce potent vasoconstriction, mediated primarily by TP receptor stimulation, and in some vessels by the release of cyclooxygenase products. This vasoconstriction may be modulated by the endothelium through the release of NO. Potent vasoconstriction is also observed with E₂-isoprostanes. Experimental and clinical data suggest a role for F₂-isoprostanes in atherogenesis. These compounds can be detected in free forms in biological fluids as well as esterified in low-density lipoproteins or cell membranes. Their quantification represents a reliable marker of lipid peroxidation. Elevated levels of F₂-isoprostanes in biological fluids in pathological conditions including atherosclerosis, ischaemia-reperfusion injury, and inflammatory vascular diseases, suggest a relationship between lipid peroxidation and such diseases. F₂-isoprostanes are currently being investigated as non-invasive quantitative markers to monitor the response to anti-oxidant treatment.

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“…Maternal cigarette smoking increased F 2 -isoprostanes in umbilical vessels (22). Vitamin C supplementation decreased iPF 2a -III in plasma from smokers (23) and nonsmokers exposed to environmental tobacco smoke (24).…”

mentioning

confidence: 99%

Quantitation of isoprostane isomers in human urine from smokers and nonsmokers by LC-MS/MS

Yan

Byrd

Ogden

2007

Journal of Lipid Research

105

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A simple, rapid liquid chromatography-tandem mass spectrometry method was developed to identify and quantitate in human urine the isoprostanes iPF 2a -III, 15-epiiPF 2a -III, iPF 2a -VI, and 8,12-iso-iPF 2a -VI along with the prostaglandin PGF 2a and 2,3-dinor-iPF 2a -III, a metabolite of iPF 2a -III. Assay specificity, linearity, precision, and accuracy met the required criteria for most analytes. The urine sample storage stability and standard solution stability were also tested.The methodology was applied to analyze 24 h urine samples collected from smokers and nonsmokers on controlled diets. The results for iPF 2a -III obtained by our method were significantly correlated with results by an ELISA, although an ?2-fold high bias was observed for the ELISA data. For iPF 2a -III and its metabolite 2,3-dinoriPF 2a -III, smokers had significantly higher concentrations than nonsmokers (513 6 275 vs. 294 6 104 pg/mg creatinine; 3,030 6 1,546 vs. 2,046 6 836 pg/mg creatinine, respectively). The concentration of iPF 2a -VI tended to be higher in smokers than in nonsmokers; however, the increase was not statistically significant in this sample set. Concentrations of the other three isoprostane isomers showed no trends toward differences between smokers and nonsmokers. Among smokers, the daily output of two type VI isoprostanes showed a weak correlation with the amount of tobacco smoke exposure, as determined by urinary excretion of total nicotine equivalents.-Yan, W., G. D. Byrd, and M. W. Ogden. Quantitation of isoprostane isomers in human urine from smokers and nonsmokers by LC-MS/MS.

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Maternal cigarette smoking increases F2-isoprostanes and reduces prostacyclin and nitric oxide in umbilical vessels

Cited by 44 publications

References 20 publications

Smoking Cessation Early in Pregnancy and Birth Weight, Length, Head Circumference, and Endothelial Nitric Oxide Synthase Activity in Umbilical and Chorionic Vessels

Smoking Cessation Early in Pregnancy and Birth Weight, Length, Head Circumference, and Endothelial Nitric Oxide Synthase Activity in Umbilical and Chorionic Vessels

Vascular Biology of the Isoprostanes

Quantitation of isoprostane isomers in human urine from smokers and nonsmokers by LC-MS/MS

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