Measuring tobacco smoke exposure: quantifying nicotine/cotinine concentration in biological samples by colorimetry, chromatography and immunoassay methods

Dhar, Preeti

doi:10.1016/j.jpba.2004.01.009

Cited by 114 publications

(64 citation statements)

References 178 publications

(212 reference statements)

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“…Extrapolation of data pertaining to cotinin levels in saliva and systemic circulation of active smokers (25), as well as nicotine content in the condensates, suggested that 0.001 to 0.003 puff/mL approximated exposure conditions in active smokers (f1 pack per day). Preliminary experiments indicated that TSC mediated modest growth inhibitory effects in A549 and Calu-6 cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

Tobacco Smoke Induces Polycomb-Mediated Repression of Dickkopf-1 in Lung Cancer Cells

et al. 2009

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Limited information is available about epigenetic mechanisms by which cigarette smoke enhances the initiation and progression of lung cancer. To examine this issue, A549 and Calu-6 lung cancer cells were cultured in normal media with or without tobacco smoke condensate (TSC) under clinically relevant exposure conditions. Ten-day TSC exposure dramatically increased the tumorigenicity of lung cancer cells in nude mice. Microarray and quantitative reverse transcription-PCR (RT-PCR) experiments revealed that this phenomenon coincided with diminished expression of Dickkopf-1 (Dkk-1). Western blot, chromatin immunoprecipitation, methylationspecific PCR, and pyrosequencing experiments showed that repression of Dkk-1 coincided with decreased H4K16Ac, increased H3K27me3, and recruitment of SirT1, EZH2, SUZ12, and Bmi1 without DNA hypermethylation within the Dkk-1 promoter despite prolonged TSC exposures. Removal of TSC from culture media resulted in loss of promoterassociated polycomb repressor complexes and reexpression of Dkk-1. siRNA-mediated knockdown of EZH2 and SirT1 partially abrogated TSC-mediated inhibition of Dkk-1 expression. Western blot and quantitative RT-PCR array experiments showed that TSC exposure as well as knockdown of Dkk-1 activated Wnt signaling and significantly up-regulated Wnt5a in lung cancer cells. Knockdown of Dkk-1 recapitulated the dramatic protumorigenic effects of TSC exposure in Calu-6 cells. Despite the transient nature of Dkk-1 repression following TSC exposure in vitro, Dkk-1 remained silenced in tumor xenografts derived from TSC-treated Calu-6 cells. Collectively, these data provide evidence that cigarette smoke directly engages polycomb machinery to activate a signaling network implicated in maintenance of cancer stem cells.

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Section: Resultsmentioning

confidence: 99%

Tobacco Smoke Induces Polycomb-Mediated Repression of Dickkopf-1 in Lung Cancer Cells

et al. 2009

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“…Moreover, Benowitz et al stated that the nicotine metabolites ratio could be used as a predictor of cigarette consumption [14]. The evaluation of xenobiotics exposure is often carried out by the immunochemical technique [15][16][17], however the chromatographic techniques are more popular due to their higher specificity [16,18]. Thin layer chromatography has been rarely used for this purpose (only to determine cotinine) [11], but the LC-MS/MS technique is frequently applied in this area [18].…”

Section: Chemicalsmentioning

confidence: 99%

Medicine students and exposure to environmental tobacco smoke

Szumska¹,

Tyrpień²,

Kowalska³

et al. 2013

International Journal of Occupational Medicine and Environmental Health

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Objective: Although medicine students express positive attitudes toward providing lifestyle counseling, they require more instruction in many areas of health behavior in order to be helpful to their patients. The presented study included the students' questionnaires analysis regarding their lifestyle and exposure to tobacco smoke. The aim of this study was to exa mine students' exposure to chosen xenobiotics by determination of selected biomarkers in urine samples, which underlay the basis for exposure assessment towards tobacco smoke. Materials and Methods: The investigated group consisted of first-and second-year medicine students from the Silesian Medical University (N = 133). Data obtained from a questionnaire survey was compared with the results of chosen biomarkers determined in urine samples. The analyses of the main nicotine metabolites were carried out firstly with use of ELISA, followed by the TLC technique with densitometry. Results: According to questionnaires, every third student examined was exposed to passive smoking. The mean concentration of the main nicotine metabolites determined by ELISA in urine samples of smoking students was 1293.52±396.70 μg/g creatinine. The results of the TLC analysis in the group of smoking students were as follows: for cotinine -523.10±68.10 μg/g creatinine and for trans-3'-hydroxycotinine -653.81±62.30 μg/g creatinine. Conclusions: Medicine students, regardless of their area of study, are a highly-exposed part of the population to tobacco smoke, not only actively but also passively. Tobacco smoke exposure can be assessed by ELISA as a screening method as well as by more specific TLC technique with densitometry.

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“…Its rate is correlated with the daily cigarettes consumption (3,4). Among all biomarkers used for routine diagnosis of in utero tobacco-smoke exposure, cotinine levels in umbilical cords are probably the most reliable and non-invasive for the newborn (5).…”

Section: Introductionmentioning

confidence: 99%

GC–MS determined cotinine in an epidemiological study on smoking status at delivery

Chazeron¹,

Daval²,

Ughetto³

et al. 2008

Pulmonary Pharmacology & Therapeutics

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A c c e p t e d m a n u s c r i p t AbstractThe objective of this study was to measure plasma cotinine levels in pregnant women and their newborns using a gas chromatography-mass spectrometry (GC-MS) method in an epidemiological delivered population with a wide range of tobacco intakes. Nearly one thousand pregnant women from regional maternity wards (n = 1007) were selected for the study. Each patient kept a tobacco diary and underwent a blood test to assess cotinine levels at the same time that newborns' cordonal plasma was taken. These values were then crosschecked.Cotinine was estimated using a selected-ion monitoring mode with a 1.5 ng/ml quantification limit. Cotinine levels in mothers and newborns were highly correlated, whatever the mother's smoking status with a calculated cut-off for cotinine levels in active smokers of 21.5 ng/ml. Finally, cotinine determined through this GC-MS method offered a sensitive and accurate measure of tobacco exposition of pregnant women and their babies.

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Measuring tobacco smoke exposure: quantifying nicotine/cotinine concentration in biological samples by colorimetry, chromatography and immunoassay methods

Cited by 114 publications

References 178 publications

Tobacco Smoke Induces Polycomb-Mediated Repression of Dickkopf-1 in Lung Cancer Cells

Tobacco Smoke Induces Polycomb-Mediated Repression of Dickkopf-1 in Lung Cancer Cells

Medicine students and exposure to environmental tobacco smoke

GC–MS determined cotinine in an epidemiological study on smoking status at delivery

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