Modulation of the mutagenic activity of cigarette smoke, cigarette smoke condensate and benzo[a]pyrene in vitro and in vivo

Mutagenesis ◽  
1994 ◽  
Vol 9 (2) ◽  
pp. 107-112 ◽  
Author(s):  
Roumen Balansky ◽  
Zvetanka Mircheva ◽  
Penka Blagoeva
Keyword(s):  
Cigarette Smoke ◽  
Mutagenic Activity ◽  
Cigarette Smoke Condensate

Humic-like substances in cigarette smoke condensate and lung tissue of smokers

1994 ◽  
Vol 266 (4) ◽  
pp. L382-L388 ◽  
Author(s):  
A. J. Ghio ◽  
J. Stonehuerner ◽  
D. R. Quigley
Keyword(s):  
Free Radical ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Cigarette Smoke Exposure ◽  
Cigarette Smoke Condensate ◽  
Free Radical Generation ◽  
Carboxylate Content ◽  
Radical Generation

Deposition of pigmented matter in the lower respiratory tract correlates with the extent of emphysema in smokers as well as with free radical generation and iron accumulation. Pulmonary emphysema is postulated to be mediated by free radical generation which is either directly or indirectly associated with cigarette smoke exposure. The hypothesis was tested that 1) incomplete combustion of tobacco yields humic-like substances (HLS) which 2) deposit in the lung as pigmented particulates, 3) complex iron cations in vitro and in vivo, and 4) have a capacity to catalyze oxidant formation. HLS, isolated by alkali extraction of cigarette smoke condensate (CSC) (Tobacco Health Research Institute, University of Kentucky), demonstrated a high carbon and low carboxylate content on elemental and functional group analyses, respectively, compared with values for HLS sequestered from soils. The HLS isolated from CSC had a capacity to complex iron in vitro and accumulated the metal in vivo after intratracheal instillation in an animal model. Both HLS and its iron complex generated free radicals, and some portion of this oxidant generation was metal dependent. Lung tissue collected at autopsy from smokers contained HLS with an infrared spectrum almost identical to that of the material isolated from CSC. Associations between particulate deposition, metal accumulation, and free radical generation suggest a possible role of HLS in the induction of lung disease following cigarette exposure.

In vitro and in vivo immunotoxic and immunomodulatory effects of nonsupplemented and selenium-supplemented cigarette smoke condensate

2004 ◽  
Vol 58 (2) ◽  
pp. 90-94 ◽  
Author(s):  
Pascale Nguyen Van Binh ◽  
Dong Zhou ◽  
Françoise Baudouin ◽  
Chantal Martin ◽  
Martine Radionoff ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Cigarette Smoke Condensate ◽  
Immunomodulatory Effects

scholarly journals Transcriptional Response of Mycobacterium tuberculosis to Cigarette Smoke Condensate

2021 ◽  
Vol 12 ◽  
Author(s):  
Danicke Willemse ◽  
Chivonne Moodley ◽  
Smriti Mehra ◽  
Deepak Kaushal
Keyword(s):  
Oxidative Stress ◽  
Mycobacterium Tuberculosis ◽  
Cigarette Smoke ◽  
Mutation Frequency ◽  
Transcriptional Response ◽  
Cigarette Smoke Condensate ◽  
Stress Survival ◽  
The Impact

Smoking is known to be an added risk factor for tuberculosis (TB), with nearly a quarter of the TB cases attributed to cigarette smokers in the 22 countries with the highest TB burden. Many studies have indicated a link between risk of active TB and cigarette smoke. Smoking is also known to significantly decrease TB cure and treatment completion rate and increase mortality rates. Cigarette smoke contains thousands of volatile compounds including carcinogens, toxins, reactive solids, and oxidants in both particulate and gaseous phase. Yet, to date, limited studies have analyzed the impact of cigarette smoke components on Mycobacterium tuberculosis (Mtb), the causative agent of TB. Here we report the impact of cigarette smoke condensate (CSC) on survival, mutation frequency, and gene expression of Mtb in vitro. We show that exposure of virulent Mtb to cigarette smoke increases the mutation frequency of the pathogen and strongly induces the expression of the regulon controlled by SigH—a global transcriptional regulator of oxidative stress. SigH has previously been shown to be required for Mtb to respond to oxidative stress, survival, and granuloma formation in vivo. A high-SigH expression phenotype is known to be associated with greater virulence of Mtb. In patients with pulmonary TB who smoke, these changes may therefore play an important, yet unexplored, role in the treatment efficacy by potentially enhancing the virulence of tubercle bacilli.

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

Studies on the mutagenic activity of ascorbic acid in vitro and in vivo

1983 ◽  
Vol 117 (1-2) ◽  
pp. 183-191 ◽  
Author(s):  
E.P. Norkus ◽  
W. Kuenzig ◽  
A.H. Conney
Keyword(s):  
Ascorbic Acid ◽  
Mutagenic Activity

scholarly journals High Levels of Dioxin-Like Potential in Cigarette Smoke Evidenced by In vitro and In vivo Biosensing

2006 ◽  
Vol 66 (14) ◽  
pp. 7143-7150 ◽  
Author(s):  
Ayumi Kasai ◽  
Nobuhiko Hiramatsu ◽  
Kunihiro Hayakawa ◽  
Jian Yao ◽  
Shuichiro Maeda ◽  
...  
Keyword(s):  
Cigarette Smoke

scholarly journals Effects of cigarette smoke condensate on the production and characterization of exopolysaccharides by Bifidobacterium

2015 ◽  
Vol 87 (2) ◽  
pp. 997-1005 ◽  
Author(s):  
Jinqiang Hu ◽  
Tao Wei ◽  
Siwen Sun ◽  
Aijing Zhao ◽  
Chunping Xu
Keyword(s):  
Cigarette Smoke ◽  
Carbohydrate Composition ◽  
Cigarette Smoke Condensate ◽  
Essential Factor ◽  
Standard Strain ◽  
Acetic Acid Production ◽  
Bifidobacterium Animalis ◽  
Molecular Determination

The aim of the study was to investigate the effect of cigarette smoke on the production and characterization of exopolysaccharides (EPSs) produced by Bifidobacterium. Cigarettes of Shanhua brand (nicotine: 1.1 mg, tar: 11 mg) were utilized to prepare a cigarette smoke condensate (CSC). The standard strain of Bifidobacterium animalis was cultured in MRS media under anaerobic addition of CSC. The results showed that CSC significantly decreased the growth of B. animalis as well as EPSs and acetic acid production. Furthermore, two EPSs fractions (Fr-I and Fr-II) were isolated and purified for chemical and molecular determination. By comparison with control, CSC was found to be of great impact on EPSs carbohydrate composition. The molecular weight mass of Fr-I changed from 3.33×105 g/mol (without CSC) to 2.99×105 (with CSC). In conclusion, in vitro studies revealed that CSC was directly able to affect the production of metabolites for B. animalis, which could be an essential factor in certain pathological disorders.

Cigarette smoking, emphysema, and damage to alpha 1-proteinase inhibitor

1994 ◽  
Vol 266 (6) ◽  
pp. L593-L611 ◽  
Author(s):  
M. D. Evans ◽  
W. A. Pryor
Keyword(s):  
Cigarette Smoke ◽  
Proteinase Inhibitor ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Lung Lavage ◽  
Tissue Destruction ◽  
Phagocytic Cells ◽  
Lung Fluid

The proteinase-antiproteinase theory for the pathogenesis of emphysema proposes that the connective tissue destruction associated with emphysema arises from excessive proteinase activity in the lower respiratory tract. For this reason, the relative activities of neutrophil elastase and alpha 1-proteinase inhibitor (alpha 1-PI) are considered important. Most emphysema is observed in smokers; therefore, alpha 1-PI has been studied as a target for smoke-induced damage. Damage to alpha 1-PI in lung fluid could occur by several mechanisms involving species delivered to the lung by cigarette smoke and/or stimulated inflammatory cells. Oxidative damage to alpha 1-PI has received particular attention, since both cigarette smoke and inflammatory cells are rich sources of oxidants. In this article we review almost two decades of research on mechanistic studies of damage to alpha 1-PI by cigarette smoke and phagocytic cells in vitro, studies emphasizing the importance of elastinolytic activity in the pathogenesis of emphysema in vivo and studies of human lung lavage fluid to detect defects in alpha 1-PI at the molecular and functional levels.

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