Comparison of Aliquot and Complete Sample Procedure for the Determination of Nicotine in Cigarette Smoke

Pillsbury, Harold C.; Bright, Colin

doi:10.1093/jaoac/55.3.636

Cited by 8 publications

(4 citation statements)

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“…CSC was prepared using the University of Kentucky Reference 3R4F Cigarettes as previously described [ 38 ]. Briefly, the particulate phase of smoke was collected on Cambridge filters using a 30-port smoking machine (Borgwaldt) under standard Federal Trade Commission conditions, [ 54 ] dissolved in DMSO at a concentration of 40 μg/ul, and stored in small aliquots at -80°C. At the time of use, aliquots were thawed in a 37°C water bath and discarded after use.…”

Section: Methodsmentioning

confidence: 99%

Exposure of Human Lung Cells to Tobacco Smoke Condensate Inhibits the Nucleotide Excision Repair Pathway

et al. 2016

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Exposure to tobacco smoke is the number one risk factor for lung cancer. Although the DNA damaging properties of tobacco smoke have been well documented, relatively few studies have examined its effect on DNA repair pathways. This is especially true for the nucleotide excision repair (NER) pathway which recognizes and removes many structurally diverse DNA lesions, including those introduced by chemical carcinogens present in tobacco smoke. The aim of the present study was to investigate the effect of tobacco smoke on NER in human lung cells. We studied the effect of cigarette smoke condensate (CSC), a surrogate for tobacco smoke, on the NER pathway in two different human lung cell lines; IMR-90 lung fibroblasts and BEAS-2B bronchial epithelial cells. To measure NER, we employed a slot-blot assay to quantify the introduction and removal of UV light-induced 6–4 photoproducts and cyclobutane pyrimidine dimers. We find a dose-dependent inhibition of 6–4 photoproduct repair in both cell lines treated with CSC. Additionally, the impact of CSC on the abundance of various NER proteins and their respective RNAs was investigated. The abundance of XPC protein, which is required for functional NER, is significantly reduced by treatment with CSC while the abundance of XPA protein, also required for NER, is unaffected. Both XPC and XPA RNA levels are modestly reduced by CSC treatment. Finally, treatment of cells with MG-132 abrogates the reduction in the abundance of XPC protein produced by treatment with CSC, suggesting that CSC enhances proteasome-dependent turnover of the protein that is mediated by ubiquitination. Together, these findings indicate that tobacco smoke can inhibit the same DNA repair pathway that is also essential for the removal of some of the carcinogenic DNA damage introduced by smoke itself, increasing the DNA damage burden of cells exposed to tobacco smoke.

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Section: Methodsmentioning

confidence: 99%

Exposure of Human Lung Cells to Tobacco Smoke Condensate Inhibits the Nucleotide Excision Repair Pathway

et al. 2016

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“…Machine yield of carbon monoxide The amount of CO formed and tar content of each cigarette type were determined under the experimental conditions under FTC conditions, reported in detail elsewhere [14], carried out at Philip Morris Product Testing Laboratories (Richmond, VA, USA). Briefly, cigarettes were smoked in a Filtrona/Cerulean Smoking Machine (Cerulean Corp., Richmond, VA, USA), models 400-450, equipped with harmonized smoking hood and CO analyser.The standard test protocol was used utilizing 35 ml puff volume over a 2-s puff duration collected every 60 s. CO was analysed in the mainstream smoke by Fourier transform infrared spectroscopy connected to the smoke machine.…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Population pharmacokinetic analysis of carboxyhaemoglobin concentrations in adult cigarette smokers

Cronenberger¹,

Mould²,

Roethig³

et al. 2007

Brit J Clinical Pharma

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WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT• The pharmacokinetics of carboxyhaemoglobin have been reported previously, primarily with regard to poisoning and toxicity.• Most of these reports have involved noncompartmental analysis of data obtained where the actual dose of carbon monoxide was not known. WHAT THIS STUDY ADDS• This study presents a comprehensive population pharmacokinetic model for carboxyhaemoglobin in adult cigarette smokers.• Since carboxyhaemoglobin is a marker of cigarette smoke exposure, model-based evaluations can be used for simulation and other evaluations of the kinetics of this agent. AIMSTo develop a population-based model to describe and predict the pharmacokinetics of carboxyhaemoglobin (COHb) in adult smokers. METHODSData from smokers of different conventional cigarettes (CC) in three open-label, randomized studies were analysed using NONMEM (version V, Level 1.1). COHb concentrations were determined at baseline for two cigarettes [Federal Trade Commission (FTC) tar 11 mg; CC1, or FTC tar 6 mg; CC2]. On day 1, subjects were randomized to continue smoking their original cigarettes, switch to a different cigarette (FTC tar 1 mg; CC3), or stop smoking. COHb concentrations were measured at baseline and on days 3 and 8 after randomization. Each cigarette was treated as a unit dose assuming a linear relationship between the number of cigarettes smoked and measured COHb percent saturation. Model building used standard methods. Model performance was evaluated using nonparametric bootstrapping and predictive checks. RESULTSThe data were described by a two-compartment model with zero-order input and first-order elimination with endogenous COHb. Model parameters included elimination rate constant (k10), central volume of distribution (Vc/F), rate constants between central and peripheral compartments (k12 and k21), baseline COHb concentrations (c0), and relative fraction of carbon monoxide absorbed (F1). The median (range) COHb half-lives were 1.6 h (0.680-2.76) and 30.9 h (7.13-367) (a and b phases, respectively). F1 increased with increasing cigarette tar content and age, whereas k12 increased with ideal body weight. CONCLUSIONA robust model was developed to predict COHb concentrations in adult smokers and to determine optimum COHb sampling times in future studies.

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“…The CSC was prepared from the University of Kentucky Reference Cigarette 1R4F (9 mg tar and 0.8 mg nicotine/cigarette). The 'tar' or particulate phase of smoke was collected on a Cambridge filter pad from cigarettes using a smoking machine set to a 35 ml puff vol of 2 s duration under standard conditions prescribed by Federal Trade Commission (14). The smoke particulate matter was dissolved in DMSO at 40 mg/ml, aliquoted into small vials and stored frozen at -80°C.…”

Section: Preparation Of Cscmentioning

confidence: 99%

Cigarette smoke condensate activates nuclear transcription factor-kappaB through phosphorylation and degradation of IkappaBalpha: correlation with induction of cyclooxygenase-2

et al. 2002

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Cigarette smoke (CS) contains several carcinogens known to initiate and promote tumorigenesis and metastasis. Because various genes that mediate carcinogenesis and tumorigenesis are regulated by nuclear factor-kappaB (NF-kappaB), we postulated that the effects of CS must be mediated through activation of this transcription factor. Therefore, in the present report we investigated whether cigarette smoke condensate (CSC) activates NF-kappaB, and whether the pathway employed for activation is similar to that of TNF, one of the potent activators of NF-kappaB. Our results show that the treatment of human histiocytic lymphoma U-937 cells with CSC activated NF-kappaB in a dose- and time-dependent manner. The kinetics of NF-kappaB activation by CSC was comparable with that of TNF. CSC-induced NF-kappaB activation was not cell type-specific, as it also activated NF-kappaB in T cells (Jurkat), lung cells (H1299), and head and neck squamous cell lines (1483 and 14B). Activation of NF-kappaB by CSC correlated with time-dependent degradation of IkappaB(alpha), an inhibitor of NF-kappaB. Further studies revealed that CSC induced phosphorylation of the serine residue at position 32 in IkappaB(alpha). In vitro immunocomplex kinase assays showed that CSC activated IkappaB(alpha) kinase (IKK). The suppression of CSC-activated NF-kappaB-dependent reporter gene expression by dominant negative form of IkappaB(alpha), TRAF2, NIK and IKK suggests a similarity to the TNF-induced pathway for NF-kappaB. CSC also induced the expression of cyclooxygenase-2, an NF-kappaB regulated gene product. Overall, our results indicate that through phosphorylation and degradation of IkappaB(alpha), CSC can activate NF-kappaB in a wide a variety of cells, and this may play a role in CS-induced carcinogenesis.

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Comparison of Aliquot and Complete Sample Procedure for the Determination of Nicotine in Cigarette Smoke

Cited by 8 publications

References 0 publications

Exposure of Human Lung Cells to Tobacco Smoke Condensate Inhibits the Nucleotide Excision Repair Pathway

Exposure of Human Lung Cells to Tobacco Smoke Condensate Inhibits the Nucleotide Excision Repair Pathway

Population pharmacokinetic analysis of carboxyhaemoglobin concentrations in adult cigarette smokers

Cigarette smoke condensate activates nuclear transcription factor-kappaB through phosphorylation and degradation of IkappaBalpha: correlation with induction of cyclooxygenase-2

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