Protective antioxidant mechanisms in rat and guinea pig tissues challenged by acute exposure to cigarette smoke

Toxicology ◽  
1992 ◽  
Vol 72 (2) ◽  
pp. 131-144 ◽  
Author(s):  
M.H. Bilimoria ◽  
D.J. Ecobichon
Keyword(s):  
Guinea Pig ◽  
Cigarette Smoke ◽  
Acute Exposure ◽  
Antioxidant Mechanisms

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.

Airway Responsiveness to Intravenous and Inhaled Acetylcholine in the Guinea Pig after Cigarette Smoke Exposure

1987 ◽  
Vol 136 (5) ◽  
pp. 1158-1162 ◽  
Author(s):  
Alan L. James ◽  
Peter Dirks ◽  
Hitoshi Ohtaka ◽  
R. Robert Schellenberg ◽  
James C. Hogg
Keyword(s):  
Guinea Pig ◽  
Cigarette Smoke ◽  
Airway Responsiveness ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure

scholarly journals Systemic effects of cigarette smoke exposure in the guinea pig

2006 ◽  
Vol 100 (7) ◽  
pp. 1186-1194 ◽  
Author(s):  
Esther Ardite ◽  
Víctor I. Peinado ◽  
Roberto A. Rabinovich ◽  
José C. Fernández-Checa ◽  
Josep Roca ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Cigarette Smoke ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Systemic Effects

scholarly journals The effect of ozone exposure on the release of eicosanoids in guinea-pig BAL fluid in relation to cellular damage and inflammation

1997 ◽  
Vol 6 (5-6) ◽  
pp. 355-361 ◽  
Author(s):  
H. J. M. Van Hoof ◽  
F. J. Zijlstra ◽  
H-P. Voss ◽  
I. M. Garrelds ◽  
J. A. M. A. Dormans ◽  
...  
Keyword(s):  
Lung Function ◽  
Inflammatory Response ◽  
Guinea Pig ◽  
Acute Exposure ◽  
Ozone Exposure ◽  
Cellular Damage ◽  
Ldh Activity ◽  
Oxidant Damage ◽  
Additional Release ◽  
Inflammatory Component

The observed effects after ozone exposure strongly depend on ozone concentration and exposure time. We hypothesized that depending on the O3exposure protocol, mainly either an oxidant damage or an inflammation will determine the O3toxicity. We compared two different ozone exposure protocols: an acute exposure (3 ppm 2 h) for studying the oxidant damage and an exposure (1 ppm 12 h) where an inflammatory component is also probably involved. We measured LDH activity and protein and albumin exudation as markers for cellular damage. After the acute exposure an increase in LDH activity was measured and after exposure to 1 ppm ozone for 12 h the exudation of protein and albumin was also enhanced. The histological examinations showed a neutrophilic inflammatory response only after exposure to 1 ppm ozone for 12 h. The acute exposure protocol resulted in an increased release of PGE2, PGD2, PGF2αand 6-ketoPGF1αwhereas exposure to 1 ppm ozone for 12 h led to an additional release of LTB4. No effects were measured on the release of TxB2and LTC4/D4/E4. These changed amounts of eicosanoids will probably contribute to the ozone-induced lung function changes.

Cigarette smoke-induced changes in guinea-pig airway responsiveness to histamine and citric acid

1991 ◽  
Vol 142 (1) ◽  
pp. 119-125 ◽  
Author(s):  
J.-A. KARLSSON ◽  
C. ZACKRISSON ◽  
C. SJÖLIN ◽  
K. FORSBERG
Keyword(s):  
Citric Acid ◽  
Guinea Pig ◽  
Cigarette Smoke ◽  
Airway Responsiveness ◽  
Induced Changes

Effects of Aclidinium Bromide in a Cigarette Smoke-Exposed Guinea Pig Model of COPD

2013 ◽  
pp. 130913081230007 ◽  
Author(s):  
David Domínguez-Fandos ◽  
Elisabet Ferrer ◽  
Raquel Puig-Pey ◽  
Cristina Carreño ◽  
Neus Prats ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Cigarette Smoke ◽  
Pig Model ◽  
Aclidinium Bromide ◽  
Guinea Pig Model

Effect of inhaled cigarette smoke on content, release and breakdown of histamine in guinea-pig lung

Life Sciences ◽  
1972 ◽  
Vol 11 (23) ◽  
pp. 1167-1171 ◽  
Author(s):  
Alan J. Lewis ◽  
Paul J. Nicholls
Keyword(s):  
Guinea Pig ◽  
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.

Sign in / Sign up

Export Citation Format

Share Document