scholarly journals Cigarette Smoke Extract Produces Superoxide in Aqueous Media by Reacting with Bicarbonate

Toxics ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 316
Author(s):  
Jung-Min Park ◽  
Haerin Jeong ◽  
Yoon-Seok Seo ◽  
Van Quan Do ◽  
Seong-Jin Choi ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Culture Media ◽  
Aqueous Media ◽  
Cigarette Smoke Extract ◽  
Experimental Conditions ◽  
Total Particulate Matter ◽  
Superoxide Formation ◽  
Cell Culture Systems ◽  
Tissue Sensitivity ◽  
Peroxy Acids

The toxicity of cigarette smoke (CS) is largely attributed to its ability to generate reactive oxygen species (ROS). Reportedly, CS generates superoxide in cell culture systems by stimulating the cells to produce superoxide and through direct chemical reactions with components of the culture media. In this study, we investigated CS-induced superoxide formation in biocompatible aqueous media and its characteristics. Cigarette smoke extract (CSE) and total particulate matter (TPM) were prepared from the mainstream smoke of 3R4F reference cigarettes. CSE and TPM generated superoxide in Hank’s balanced salt solution (HBSS), Dulbecco’s modified Eagle media (DMEM), and blood plasma, but not in distilled water and phosphate-buffered saline. Each constituent of HBSS in solution was tested, and bicarbonate was found to be responsible for the superoxide generation. More than half of the superoxide formation was abolished by pretreating CSE or TPM with peroxidase, indicating that the substrates of peroxidase, presumably peroxides and peroxy acids, mainly contributed to the superoxide production. In conclusion, the presence of bicarbonate in experimental conditions should be considered carefully in studies of the biological activity of CS. Furthermore, the local amount of bicarbonate in exposed tissues may be a determinant of tissue sensitivity to oxidative damage by CS.

scholarly journals Differential Effects between Cigarette Total Particulate Matter and Cigarette Smoke Extract on Blood and Blood Vessel

2016 ◽  
Vol 32 (4) ◽  
pp. 353-358 ◽  
Author(s):  
Jung-Min Park ◽  
Kyung-Hwa Chang ◽  
Kwang-Hoon Park ◽  
Seong-Jin Choi ◽  
Kyuhong Lee ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Blood Vessel ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Total Particulate Matter ◽  
Differential Effects

Alveolar epithelial cells type II show a high sensitivity to cigarette smoke extract

Pneumologie ◽  
2014 ◽  
Vol 68 (06) ◽  
Author(s):  
S Seehase ◽  
B Baron-Luehr ◽  
C Kugler ◽  
E Vollmer ◽  
T Goldmann
Keyword(s):  
Epithelial Cells ◽  
Cigarette Smoke ◽  
High Sensitivity ◽  
Cigarette Smoke Extract ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Alveolar Epithelial

The Control of Cigarette Smoke Deliveries Using Heat-Shrinkable Films

1975 ◽  
Vol 8 (2) ◽  
Author(s):  
R. A. Crellin ◽  
G. O. Brooks ◽  
H. G. Horsewell
Keyword(s):  
Particulate Matter ◽  
Cellulose Acetate ◽  
Cigarette Smoke ◽  
Total Particulate Matter ◽  
Puff Volume ◽  
Cigarette Paper ◽  
High Degree

AbstractA ventilating filter for cigarettes has been developed which reduces the delivery of smoke constituents from the final two to three puffs. Since the normaI delivery for these three puffs can account for up to half the total particulate matter and nicotine delivered by the whole cigarette, usefuI reductions per cigarette can be produced. The ventilating filter consists of cellulose acetate tow wrapped in heat-shrinkable film and attached to a tobacco rod using perforated tipping paper. When the cigarette is smoked, the perforations remain closed by contact with the impermeable film until transfer of heat to the filter is sufficient to soften the filter tow and shrink the film. Ventilating air now enters the cigarette and reduces the smoke deliveries. The effectiveness of the ventilating filter is increased by using films which have a low shrink temperature, high shrink tension and a high degree of biaxiaI shrinkage. Increases in filter plasticiser level, tipping perforation area and puff volume improve the effectiveness of the ventilating filter but increases in cigarette paper porosity and tobacco butt length reduce the effectiveness

Dysregulation of gastric H,K-ATPase by cigarette smoke extract

2009 ◽  
Vol 15 (32) ◽  
pp. 3416
Author(s):  
Muna Hammadi ◽  
Mohamed Adi ◽  
Rony John ◽  
Ghalia AK Khoder ◽  
Sherif M Karam
Keyword(s):  
Cigarette Smoke ◽  
Cigarette Smoke Extract

scholarly journals Extracellular vesicles from human airway basal cells respond to cigarette smoke extract and affect vascular endothelial cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ashish Saxena ◽  
Matthew S. Walters ◽  
Jae-Hung Shieh ◽  
Ling-Bo Shen ◽  
Kazunori Gomi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cigarette Smoke ◽  
Extracellular Vesicles ◽  
Basal Cell ◽  
Mapk Signaling ◽  
Cigarette Smoke Extract ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Basal Cells ◽  
Human Airway

AbstractThe human airway epithelium lining the bronchial tree contains basal cells that proliferate, differentiate, and communicate with other components of their microenvironment. One method that cells use for intercellular communication involves the secretion of exosomes and other extracellular vesicles (EVs). We isolated exosome-enriched EVs that were produced from an immortalized human airway basal cell line (BCi-NS1.1) and found that their secretion is increased by exposure to cigarette smoke extract, suggesting that this stress stimulates release of EVs which could affect signaling to other cells. We have previously shown that primary human airway basal cells secrete vascular endothelial growth factor A (VEGFA) which can activate MAPK signaling cascades in endothelial cells via VEGF receptor–2 (VEGFR2). Here, we show that exposure of endothelial cells to exosome-enriched airway basal cell EVs promotes the survival of these cells and that this effect also involves VEGFR2 activation and is, at least in part, mediated by VEGFA present in the EVs. These observations demonstrate that EVs are involved in the intercellular signaling between airway basal cells and the endothelium which we previously reported. The downstream signaling pathways involved may be distinct and specific to the EVs, however, as increased phosphorylation of Akt, STAT3, p44/42 MAPK, and p38 MAPK was not seen following exposure of endothelial cells to airway basal cell EVs.

scholarly journals Loss of IL-33 enhances elastase-induced and cigarette smoke extract-induced emphysema in mice

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Daisuke Morichika ◽  
Akihiko Taniguchi ◽  
Naohiro Oda ◽  
Utako Fujii ◽  
Satoru Senoo ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Intratracheal Instillation ◽  
Inflammatory Cells ◽  
Cigarette Smoke Extract ◽  
Lymphoid Cells ◽  
Chronic Obstructive ◽  
Porcine Pancreas ◽  
Obstructive Pulmonary Disease ◽  
Quantitative Morphometry ◽  
Cytokines And Chemokines

Abstract Background IL-33, which is known to induce type 2 immune responses via group 2 innate lymphoid cells, has been reported to contribute to neutrophilic airway inflammation in chronic obstructive pulmonary disease. However, its role in the pathogenesis of emphysema remains unclear. Methods We determined the role of interleukin (IL)-33 in the development of emphysema using porcine pancreas elastase (PPE) and cigarette smoke extract (CSE) in mice. First, IL-33−/− mice and wild-type (WT) mice were given PPE intratracheally. The numbers of inflammatory cells, and the levels of cytokines and chemokines in the bronchoalveolar lavage (BAL) fluid and lung homogenates, were analyzed; quantitative morphometry of lung sections was also performed. Second, mice received CSE by intratracheal instillation. Quantitative morphometry of lung sections was then performed again. Results Intratracheal instillation of PPE induced emphysematous changes and increased IL-33 levels in the lungs. Compared to WT mice, IL-33−/− mice showed significantly greater PPE-induced emphysematous changes. No differences were observed between IL-33−/− and WT mice in the numbers of macrophages or neutrophils in BAL fluid. The levels of hepatocyte growth factor were lower in the BAL fluid of PPE-treated IL-33−/− mice than WT mice. IL-33−/− mice also showed significantly greater emphysematous changes in the lungs, compared to WT mice, following intratracheal instillation of CSE. Conclusion These observations suggest that loss of IL-33 promotes the development of emphysema and may be potentially harmful to patients with COPD.

Pirfenidone mediates cigarette smoke extract induced inflammation and oxidative stress in vitro and in vivo

2021 ◽  
Vol 96 ◽  
pp. 107593
Author(s):  
Yiming Ma ◽  
Lijuan Luo ◽  
Xiangming Liu ◽  
Herui Li ◽  
Zihang Zeng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
And Oxidative Stress

scholarly journals Acute electronic vapour product whole aerosol exposure of 3D human bronchial tissue results in minimal cellular and transcriptomic responses when compared to cigarette smoke

2021 ◽  
Vol 5 ◽  
pp. 239784732098849
Author(s):  
Gary Phillips ◽  
Lukasz Czekala ◽  
Holger P Behrsing ◽  
Khalid Amin ◽  
Jessica Budde ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Recovery Time ◽  
Beat Frequency ◽  
Transcriptomic Response ◽  
Potential Harm ◽  
Aerosol Exposure ◽  
Cell Culture Systems ◽  
Computational Sciences ◽  
Potential Risks ◽  
Reduced Toxicity

The use of electronic vapour products (EVPs) continues to increase worldwide and with advances in cell culture systems, molecular biology and the computational sciences there is also accumulating evidence of their potential reduced toxicity and reduced potential harm when compared to cigarette smoke. To further understand the potential risks and health effects associated with exposure to EVP aerosols we have assessed the cellular and transcriptomic response from a commercially available lung tissue culture system (MucilAirTM) following a single sub-cytotoxic exposure to cigarette smoke and the equivalent nicotine delivered dose of EVP aerosol. The transcriptomic, cellular (cilia beat frequency (CBF) and percent active area (%AA), trans epithelial electrical resistance (TEER), histology) and cytokine release were assessed at 4- and 48- hours following recovery from air, EVP aerosol (8.4% V/V: mybluTM blueberry flavour, 2.4% nicotine) and 3R4F smoke (3.5% V/V: exposure). No pathological changes were observed at either recovery time point from any exposure. Air and EVP aerosol exposure had no effect on CBF, %AA nor TEER at 48 hours. Exposure to cigarette smoke resulted in a decrease in TEER, an increase in CBF and the release of proinflammatory cytokines at both recovery time points. Although the number of significantly expressed genes was minimal following exposure to EVP aerosol, exposure to 3R4F smoke resulted in a significant upregulation of several disease relevant pathways. These data provide evidence that following an acute exposure to EVP aerosol there is significantly less damage to lung cells in culture than the equivalent, nicotine based, dose of cigarette smoke.

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