Murine lung tumor response after exposure to cigarette mainstream smoke or its particulate and gas/vapor phase fractions

Stinn, Walter; Arts, J.H.E.; Buettner, Ansgar; Duistermaat, Evert; Janssens, Kris; Kuper, C. Frieke; Haussmann, Hans-Juergen

doi:10.1016/j.tox.2010.05.005

Cited by 26 publications

(26 citation statements)

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“…Major design features of this whole-body MS inhalation, such as smoking machine and exposure conditions, were as previously described (Stinn et al ., 2010). Total particulate matter (TPM) concentrations in this study were slightly higher, i.e., 150mg/m 3 (MS-150) and 300mg/m 3 (MS-300).…”

Section: Methodsmentioning

confidence: 99%

“…Previous MS inhalation studies with A/J mice were positive for lung tumors in some laboratories but not in others (Stinn et al ., 2010); this may be due to differences in study design parameters such as sufficiently large group sizes or the exposure schedule. All positive studies so far have adhered to a schedule involving several months of MS inhalation followed by a postinhalation period without exposure for several months, which has been adapted from the positive lung tumorigenesis studies with ETSS (Witschi, 2005).…”

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confidence: 95%

“…In the past, attempts to establish such models were generally unsuccessful (reviewed by Coggins [2010]), for reasons not fully understood. More recently, however, some chronic MS inhalation studies with mice or rats that followed specific design considerations were positive in demonstrating lung tumor formation (Balansky et al ., 2007; Curtin et al ., 2004; Gordon and Bosland, 2009; Hutt et al ., 2005; Mauderly et al ., 2004; Stinn et al ., 2010). …”

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confidence: 99%

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Lung Inflammatory Effects, Tumorigenesis, and Emphysema Development in a Long-Term Inhalation Study with Cigarette Mainstream Smoke in Mice

Stinn¹,

Buettner²,

Weiler³

et al. 2012

Toxicological Sciences

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Cigarette smoking is the leading cause of lung cancer and chronic obstructive pulmonary disease, yet there is little mechanistic information available in the literature. To improve this, laboratory models for cigarette mainstream smoke (MS) inhalation–induced chronic disease development are needed. The current study investigated the effects of exposing male A/J mice to MS (6h/day, 5 days/week at 150 and 300mg total particulate matter per cubic meter) for 2.5, 5, 10, and 18 months in selected combinations with postinhalation periods of 0, 4, 8, and 13 months. Histopathological examination of step-serial sections of the lungs revealed nodular hyperplasia of the alveolar epithelium and bronchioloalveolar adenoma and adenocarcinoma. At 18 months, lung tumors were found to be enhanced concentration dependently (up to threefold beyond sham exposure), irrespective of whether MS inhalation had been performed for the complete study duration or was interrupted after 5 or 10 months and followed by postinhalation periods. Morphometric analysis revealed an increase in the extent of emphysematous changes after 5 months of MS inhalation, which did not significantly change over the following 13 months of study duration, irrespective of whether MS exposure was continued or not. These changes were found to be accompanied by a complex pattern of transient and sustained pulmonary inflammatory changes that may contribute to the observed pathogeneses. Data from this study suggest that the A/J mouse model holds considerable promise as a relevant model for investigating smoking-related emphysema and adenocarcinoma development.

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Section: Methodsmentioning

confidence: 99%

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confidence: 95%

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confidence: 99%

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Lung Inflammatory Effects, Tumorigenesis, and Emphysema Development in a Long-Term Inhalation Study with Cigarette Mainstream Smoke in Mice

Stinn¹,

Buettner²,

Weiler³

et al. 2012

Toxicological Sciences

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“…However, in the case of nicotine-and tar-free CSE, it is difficult to express its concentration, because it does not contain appropriate endogenous substances like nicotine and tar. In this context, most researchers represent the concentration by the number of cigarettes used for CSE preparation 16,[30][31][32] or the number of puffs. [33][34][35][36] Other researchers represent the concentration in terms of the optical density at 302 nm (OD).…”

Section: Expression Of the Concentration Of Csementioning

confidence: 99%

A Standardized Method for the Preparation of a Gas Phase Extract of Cigarette Smoke

Higashi

Mai

Mazaki

et al. 2016

Biological & Pharmaceutical Bulletin

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The gas phase of cigarette smoke is important from the viewpoint of human health, because it can pass through alveolar epithelium and enter the circulation. There is no standard method for the preparation of a gas phase extract of cigarette smoke (CSE), although CSE is widely used for research instead of whole cigarette smoke. We have established a standard method for the preparation of CSE. One cigarette per trial is continuously combusted under a reduced pressure generated by an aspiration pump with a velocity of 1.050 L/min: the main stream of the smoke is passed through a Cambridge filter to remove tar, and subsequently, bubbled through a glass ball filter (pore size, 20-30 µm) into 15 mL of phosphate-buffered saline (PBS). To express the concentration of CSE, a virtual tar concentration is introduced, which is calculated assuming that tar trapped on the Cambridge filter is dissolved in the PBS. CSEs prepared from smaller numbers of cigarettes (original virtual tar concentration≤15 mg/mL) show similar concentration-response curves for cytotoxicity versus virtual tar concentrations. CSEs prepared from various brands of cigarettes and by different smoking regimes (continuous and puff smoking) show similar cytotoxic potency if the virtual tar concentrations are the same. In conclusion, using the standardized method for CSE preparation in combination with the virtual tar concentration, it becomes possible to simply and rapidly prepare standard CSEs with defined concentrations from any brand of cigarettes, which are toxicologically equivalent to CSE prepared by puff smoking.

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“…The air pollution with respect to particulates caused by cigarette smoking can be 10 times greater than that caused by an idling diesel car (Invernizzi et al 2004). Tobacco-specific nitrosamines (TSNAs) are toxic compounds present in cigarette smoke and tobacco products (Chen et al 2008;Hecht and Hoffmann 1988;Stinn et al 2010). Specifically, 4-(methyl nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent pulmonary carcinogen, reported by the International Agency for Research on Cancer as a human carcinogen (IARC 2007), and exerts a wide spectrum of biological effects on the lung and lung airways, including oxidative stress, inflammation, and deoxyribonucleic acid (DNA) damage (Hecht and Hoffmann 1988;Lin et al 2010;Tyroller et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Impaired phospholipid metabolism inSaccharomyces cerevisiaeby increased phospholipase B activity induced by 4-(methyl nitrosamino)-1-(3-pyridyl)-1-butanone

Vijayaraj

Jayaraja

Nachiappan

2011

Toxicological & Environmental Chemistry

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Tobacco products and cigarette smoke cause many respiratory diseases including cancer. 4-(Methyl nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a potent carcinogen in cigarette smoke, but its effect on lipid metabolism remains enigmatic. Hence, Saccharomyces cerevisiae was exposed to different concentrations of NNK (0-400 mmol L À1 ) to elucidate its role in lipid metabolism. Exposure to NNK substantially decreases (about 60%) of the phospholipid content with a concomitant increase in lysophospholipids. Significant reduction was observed in the phosphatidylcholine followed by phosphatidylethanolamine with NNKtreated cells. On the contrary, cells accumulated significant amount of neutral lipids and free fatty acids. Exposure of yeast cells (wild-type cells and three plbD mutant strains) to NNK greatly enhances the hydrolysis of phospholipid in the presence of calcium. We are the first to report that exposure to NNK enhances phospholipase B (PLB), particularly plb1p activity. Furthermore, NNK also promotes the alteration of phospholipid fatty acid (FA) content. These results suggest that NNK aids in the degradation of phospholipids by enhanced PLB activity and is accompanied with FA alteration. Understanding the altered phospholipid metabolism in the presence of NNK remains a worthy pursuit.

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Murine lung tumor response after exposure to cigarette mainstream smoke or its particulate and gas/vapor phase fractions

Cited by 26 publications

References 50 publications

Lung Inflammatory Effects, Tumorigenesis, and Emphysema Development in a Long-Term Inhalation Study with Cigarette Mainstream Smoke in Mice

Lung Inflammatory Effects, Tumorigenesis, and Emphysema Development in a Long-Term Inhalation Study with Cigarette Mainstream Smoke in Mice

A Standardized Method for the Preparation of a Gas Phase Extract of Cigarette Smoke

Impaired phospholipid metabolism inSaccharomyces cerevisiaeby increased phospholipase B activity induced by 4-(methyl nitrosamino)-1-(3-pyridyl)-1-butanone

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