Effects of the intranasal application of gold nanoparticles on the pulmonary tissue after acute exposure to industrial cigarette smoke

2021 ◽  
Author(s):  
Germano Duarte Porto ◽  
Daniela Pacheco dos Santos Haupenthal ◽  
Priscila Soares Souza ◽  
Gustavo de Bem Silveira ◽  
Renata Tiscoski Nesi ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Cigarette Smoke ◽  
Acute Exposure ◽  
Pulmonary Tissue ◽  
Intranasal Application

Pulmonary tissue and cigarette smoke

1983 ◽  
Vol 31 (1) ◽  
pp. 176-188 ◽  
Author(s):  
Daniel H. Matulionis
Keyword(s):  
Cigarette Smoke ◽  
Pulmonary Tissue

Endothelial and left ventricular diastolic function in young adults exposed to tobacco

2019 ◽  
Vol 97 (10) ◽  
pp. 1006-1011
Author(s):  
Ayelen Rodriguez-Portelles ◽  
Delfin Rodriguez-Leyva
Keyword(s):  
Young Adults ◽  
Flow Velocity ◽  
Diastolic Function ◽  
Cigarette Smoke ◽  
Brachial Artery ◽  
Left Ventricular Diastolic Function ◽  
Left Ventricular ◽  
Acute Exposure ◽  
Brachial Artery Diameter ◽  
Arterial Dilation

Smoking is associated with endothelial and left ventricular diastolic disfunction. We aimed to determine the endothelial and diastolic function in young adults exposed to tobacco smoke and the effects of acute exposure to it. Smokers were considered as cases and non-smokers as controls. Brachial artery diameter, brachial artery flow velocity, and echocardiographic variables were measured. Mean age of the participants was 21 years. Smokers showed significant endothelial dysfunction compared with non-smokers. Arterial dilation mediated by the endothelium was significantly higher in non-smokers than in smokers (p = 0.005). Non-endothelium-mediated arterial dilation was significantly impaired in smokers compared with non-smokers (p = 0.02). After reactive hyperaemia, there was a significant increase in blood flow in non-smokers (61%) compared with that in smokers (29%). Acute cigarette exposure showed a trend towards left ventricle diastolic disfunction in smokers. Left atrium diameter was significantly higher in smokers than in non-smokers. After acute exposure to cigarette smoke, arterial dilation and brachial flow velocity were lower than those achieved in the abstinence phase (p = 0.005). We concluded that endothelium-dependent arterial dilation is impaired in young smokers and it worsens even after acute exposure to cigarette smoke.

scholarly journals Impact of acute exposure to cigarette smoke on airway gene expression

2018 ◽  
Vol 50 (9) ◽  
pp. 705-713 ◽  
Author(s):  
E. Billatos ◽  
A. Faiz ◽  
Y. Gesthalter ◽  
A. LeClerc ◽  
Y. O. Alekseyev ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Lung Cancer ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Acute Exposure ◽  
Cigarette Smoke Exposure ◽  
Airway Epithelial ◽  
Long Term Effects ◽  
Chronic Smoking

Background: Understanding effects of acute smoke exposure (ASE) on airway epithelial gene expression and their relationship with the effects of chronic smoke exposure may provide biological insights into the development of smoking-related respiratory diseases. Methods: Bronchial airway epithelial cell brushings were collected from 63 individuals without recent cigarette smoke exposure and before and 24 h after smoking three cigarettes. RNA from these samples was profiled on Affymetrix Human Gene 1.0 ST microarrays. Results: We identified 91 genes differentially expressed 24 h after ASE (false discovery rate < 0.25). ASE induced genes involved in xenobiotic metabolism, oxidative stress, and inflammation and repressed genes related to cilium morphogenesis and cell cycle. While many genes altered by ASE are altered similarly in chronic smokers, metallothionein genes are induced by ASE and suppressed in chronic smokers. Metallothioneins are also suppressed in current and former smokers with lung cancer relative to those without lung cancer. Conclusions: Acute exposure to as little as three cigarettes and chronic smoking induce largely concordant changes in airway epithelial gene expression. Differences in short-term and long-term effects of smoking on metallothionein expression and their relationship to lung cancer requires further study given these enzymes’ role in the oxidative stress response.

scholarly journals Acute cigarette smoke inhalation blunts lung responsiveness to methacholine and allergen in rabbit: differentiation of central and peripheral effects

2010 ◽  
Vol 299 (2) ◽  
pp. L242-L251 ◽  
Author(s):  
Liisa Porra ◽  
Ferenc Peták ◽  
Satu Strengell ◽  
Kimmo Neitola ◽  
Tibor Z. Janosi ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Airway Responsiveness ◽  
Smoke Inhalation ◽  
Acute Exposure ◽  
Tobacco Smoke Exposure ◽  
Short Term ◽  
Peripheral Airway ◽  
Airway Response ◽  
Central Airway ◽  
Mainstream Cigarette Smoke

Despite the prevalence of active smoking in asthmatics, data on the short-term effect of acute mainstream tobacco smoke exposure on airway responsiveness are very scarce. The aim of this study was to assess the immediate effect of acute exposure to mainstream cigarette smoke on airway reactivity to subsequent nonspecific and allergenic challenges in healthy control ( n = 5) and ovalbumin-sensitized rabbits ( n = 6). We combined low-frequency forced oscillations and synchrotron radiation CT imaging to differentiate central airway and peripheral airway and lung parenchymal components of the response to airway provocation. Acute exposure to smoke generated by four successive cigarettes (CS) strongly inhibited the central airway response to subsequent IV methacholine (MCh) challenge. In the sensitized animals, although the response to ovalbumin was also inhibited in the central airways, mainstream CS did not blunt the peripheral airway response in this group. In additional groups of experiments, exposure to HEPA-filtered CS ( n = 6) similarly inhibited the MCh response, whereas CO (10,000 ppm for 4 min, n = 6) or nitric oxide inhalation instead of CS (240 ppm, 4 × 7 min, n = 5) failed to blunt nonspecific airway responsiveness. Pretreatment with α-chymotrypsin to inhibit endogenous VIP before CS exposure had no effect ( n = 4). Based on these observations, the gas phase of mainstream cigarette smoke may contain one or more short-term inhibitory components acting primarily on central airways and inhibiting the response to both specific and nonspecific airway provocation, but not on the lung periphery where both lung mechanical parameters, and synchrotron-imaging derived parameters, showed large changes in response to allergen challenge in sensitized animals.

No overt structural or functional changes associated with PEG-coated gold nanoparticles accumulation with acute exposure in the mouse heart

2013 ◽  
Vol 222 (2) ◽  
pp. 197-203 ◽  
Author(s):  
Chengzhi Yang ◽  
Hui Yang ◽  
Jimin Wu ◽  
Zenghui Meng ◽  
Rui Xing ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Acute Exposure ◽  
Mouse Heart ◽  
Functional Changes
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