A Simple and Rapid Method for Standard Preparation of Gas Phase Extract of Cigarette Smoke

@article{Higashi2014ASA,
  title={A Simple and Rapid Method for Standard Preparation of Gas Phase Extract of Cigarette Smoke},
  author={T. Higashi and Y. Mai and Y. Noya and T. Horinouchi and K. Terada and A. Hoshi and Prabha Nepal and T. Harada and Mika Horiguchi and Chizuru Hatate and Y. Kuge and S. Miwa},
  journal={PLoS ONE},
  year={2014},
  volume={9}
}
Cigarette smoke consists of tar and gas phase: the latter is toxicologically important because it can pass through lung alveolar epithelium to enter the circulation. Here we attempt to establish a standard method for preparation of gas phase extract of cigarette smoke (CSE). CSE was prepared by continuously sucking cigarette smoke through a Cambridge filter to remove tar, followed by bubbling it into phosphate-buffered saline (PBS). An increase in dry weight of the filter was defined as tar… Expand
A Standardized Method for the Preparation of a Gas Phase Extract of Cigarette Smoke.
TLDR
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. Expand
Carbonyl Compounds in the Gas Phase of Cigarette Mainstream Smoke and Their Pharmacological Properties.
TLDR
Pharmacological modulation of PKC and NOX activities and the trapping of ROS are potential strategies for the prevention of diseases related to cigarette smoking. Expand
A Simple, Inexpensive and Adaptable Smoke Extraction System
Tobacco smoking and exposure to biomass smoke are the major sources of exposure to harmful chemicals and particulate matter which may lead to cardiovascular and lung diseases. Our understanding ofExpand
Determination of eight carbonyl compounds in aerosols trapped in phosphate buffer saline solutions to support in vitro assessment studies.
TLDR
Validation results confirmed that the established working ranges also allow the analysis of THS aerosols, where the concentrations of carbonyl compounds are substantially lower than those generated by 3R4F cigarettes. Expand
Glutathione and cysteines suppress cytotoxicity of gas phase of cigarette smoke by direct reacting with unsaturated carbonyl compounds in the gas phase.
TLDR
The current results suggest that GSH, NAC, and cysteines directly reacted with ACR and MVK, and suppressed these unsaturated carbonyl compounds-induced cell damage by inhibition of protein carbonylation. Expand
Cigarette Smoke Extract Induces Ferroptosis in Vascular Smooth Muscle Cells.
TLDR
It is demonstrated that ferroptosis is responsible for CSE-induced VSMC death and suggest that ferROPTosis is a potential therapeutic target for preventing aortic aneurysm and dissection. Expand
Invasion-inhibiting Effects of Gaseous Components in Cigarette Smoke on Mouse Rectal Carcinoma Colon-26 Cells.
TLDR
The action of methyl vinyl ketone (MVK) on the invasiveness of Colon-26 cells was examined to identify the active component in CSE and it was found that MVK may be a candidate active component of CSE. Expand
Intracellular Metabolism of α,β-Unsaturated Carbonyl Compounds, Acrolein, Crotonaldehyde and Methyl Vinyl Ketone, Active Toxicants in Cigarette Smoke: Participation of Glutathione Conjugation Ability and Aldehyde-Ketone Sensitive Reductase Activity.
TLDR
The results show that the GSH adducts of α,β-unsaturated aldehydes, CA and ACR, are quickly reduced by certain intracellular carbonyl reductase(s) and excreted from the cells, unlike the G SH-MVK adduct, which might be related to differences in the cytotoxicity ofα, β-uns saturated aldeHydes and ketones. Expand
Neutrophil Extracellular Traps Stimulate Proinflammatory Responses in Human Airway Epithelial Cells
TLDR
The findings indicate that NET exert direct proinflammatory effects on airway epithelial cells that might contribute in vivo to the further recruitment of neutrophils and the perpetuation of inflammation upon lung tissue damage. Expand
ShenqiBufei attenuates chronic obstructive pulmonary disease
Objective: To evaluate the therapeutic effect of Chinese medicine ShenqiBufei (SBF) onchronic obstructive pulmonary disease (COPD) in a rat COPD model. Methods: SBF was prepared from Astragalus,Expand
...
1
2
...

References

SHOWING 1-10 OF 40 REFERENCES
Identification of stable cytotoxic factors in the gas phase extract of cigarette smoke and pharmacological characterization of their cytotoxicity.
TLDR
Results show that acrolein and MVK areresponsible for the acute cytotoxicity of the CSE through PKC/NOX-dependent and -independent mechanisms, whereas CPO is responsible for the delayed cytot toxicity of theCSE through a PKC or NOX-independent mechanism. Expand
Oxidants in the gas phase of cigarette smoke pass through the lung alveolar wall and raise systemic oxidative stress.
TLDR
It is demonstrated that relatively stable oxidants in CSE can pass through the pulmonary alveolar wall into the blood and induce systemic oxidative stress, which most likely facilitates oxidative modification of LDL and endothelial dysfunction, explaining early key events in the development of atherosclerosis. Expand
Possible existence of platelet aggregation inhibitor(s) in a gas-phase extract of cigarette smoke.
TLDR
The facts suggest that the anti-platelet substance in the water extract of cigarette smoke seems to be moderately non polar, both acidic and basic in water and not adsorbed by hemoglobin. Expand
Cigarettes and cigarette smoking.
  • D. Burns
  • Medicine
  • Clinics in chest medicine
  • 1991
TLDR
The irritant agents in the smoke cause acute and chronic changes in lung structure and function that may result in greater retention of carcinogens within the lung and increased vulnerability of the lung to the effects of these carcinogens. Expand
Gas phase oxidants of cigarette smoke induce lipid peroxidation and changes in lipoprotein properties in human blood plasma. Protective effects of ascorbic acid.
TLDR
The results support the concept of an increased vitamin C utilization in smokers, and suggest that lipid peroxidation induced by oxidants present in the gas phase of CS leads to potentially atherogenic changes in lipoproteins. Expand
Acrolein in cigarette smoke inhibits T-cell responses.
TLDR
The vapor phase from cigarette smoke extracts potently suppresses cytokine production, and the compound responsible for this inhibition appears to be acrolein. Expand
Some consequences of using cigarette machine smoking regimes with different intensities on smoke yields and their variability.
TLDR
Yield data from the intense regime may not reflect the effectiveness of cigarette design features to reduce certain smoke components that occurs when products are smoked under conditions closer to those used by the majority of smokers in real world situations, implying that higher tolerances may need to be set and taken into account when smoking under the intense regimes. Expand
Cigarette smoke-induced proinflammatory alterations in the endothelial phenotype: role of NAD(P)H oxidase activation.
TLDR
It is proposed that water-soluble components of cigarette smoke activate the vascular NAD(P)H oxidase, leading to proinflammatory alterations in vascular phenotype, which likely promotes development of atherosclerosis, especially if other risk factors are also present. Expand
Dependence of tar, nicotine and carbon monoxide yields on physical parameters: implications for exposure, emissions control and monitoring
TLDR
Yields are predictable with reasonable accuracy and precision using only measured physical parameters, and surrogate exposure indicators suggest that filter ventilation does not lead to any reduction in exposure and that highly ventilated (low-yield) brands may actually increase exposure to the more volatile toxins. Expand
Preneoplastic and neoplastic lesions in the lung, liver and urinary tract of mice exposed to environmental cigarette smoke and UV light since birth
TLDR
Exposure to environmental CS for 120 days, starting within 12 hr after birth, resulted in an early appearance of preneoplastic lesions in lung, which however tended to attenuate after discontinuing exposure, and induction by ECS of alterations in the urinary tract were unrelated to the exposure time after birth. Expand
...
1
2
3
4
...