Document Detail


Exercise may offset nicotine-induced injury in lung tissue: a preliminary histological study based on a rat model.
MedLine Citation:
PMID:  22452750     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Nicotine appears to be the primary pharmacologic agent that causes smoking-related pulmonary diseases. An understanding of the effect of nicotine on lungs is essential to develop interventions that can be used to counter smoking-related diseases. Further, it is shown that physical exercise may partially reverse smoking-induced pathological changes in experimental animals. Hence, this study focuses on the pathological changes in rat lung following nicotine administration and the role of exercise in reversing the nicotine-induced lung injury. This is a randomized controlled trial with 3 groups of rats. Control (CG), nicotine-exposed (NG), and nicotine-exposed and exercise group (NEG). Control group received no intervention. Both NG and NEG were given 1.5 mg/kg nicotine base, daily, subcutaneously, but NEG were also subjected to an intensive daily swimming protocol. The rats were sacrificed and the lung tissue was processed for light and transmission electron microscopic and immunohistochemical studies. Compared with the control group, the nicotine group showed enlargement and destruction of the alveolar septum, cellular hyperplasia and interstitial fibrosis, and interstitial mononuclear cell infiltration with increased intraluminal macrophages. There was only modest morphological change between the nicotine administered and nicotine and exercise groups. Expression of superoxide dismutase (SOD) and catalase showed a mild increase in the NEG, whereas glutathione peroxidase (GPX) showed mild and moderate increase in the expression in the NG and NEG, respectively. This study shows that nicotine induces substantial pathological changes in the lung and prolonged exercise may have some beneficial effects in partially reversing the nicotine-induced lung injury by inducing the expression of antioxidants.
Authors:
S Al-Obaidi; T C Mathew; E Dean
Publication Detail:
Type:  Journal Article     Date:  2012-03-27
Journal Detail:
Title:  Experimental lung research     Volume:  38     ISSN:  1521-0499     ISO Abbreviation:  Exp. Lung Res.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-04-05     Completed Date:  2012-08-02     Revised Date:  2012-11-29    
Medline Journal Info:
Nlm Unique ID:  8004944     Medline TA:  Exp Lung Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  211-21     Citation Subset:  IM    
Affiliation:
Department of Physical Therapy, Faculty of Allied Health Sciences, Kuwait University, Kuwait.
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MeSH Terms
Descriptor/Qualifier:
Animals
Catalase / metabolism
Disease Models, Animal
Glutathione Peroxidase / metabolism
Immunohistochemistry
Lung / metabolism,  pathology
Lung Injury / etiology,  metabolism,  pathology,  prevention & control*
Male
Microscopy, Electron, Transmission
Nicotine / toxicity*
Physical Exertion / physiology*
Rats
Rats, Wistar
Smoking / adverse effects,  pathology
Superoxide Dismutase / metabolism
Chemical
Reg. No./Substance:
54-11-5/Nicotine; EC 1.11.1.6/Catalase; EC 1.11.1.9/Glutathione Peroxidase; EC 1.15.1.1/Superoxide Dismutase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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