title: Exercise may offset nicotine-induced injury in lung tissue: a preliminary histological study based on a rat model.
abstract: 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.affiliation: Department of Physical Therapy, Faculty of Allied Health Sciences, Kuwait University, Kuwait.
authors.forename: S
authors.initials: S
authors.lastname: Al-Obaidi
authors.forename: T C
authors.initials: TC
authors.lastname: Mathew
authors.forename: E
authors.initials: E
authors.lastname: Dean
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D005979:Glutathione Peroxidase / Q000378:metabolism; D007150:Immunohistochemistry; D008168:Lung / Q000378:metabolism / Q000473:pathology; D055370:Lung Injury / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D046529:Microscopy, Electron, Transmission; D009538:Nicotine / Q000633:toxicity*; D005082:Physical Exertion / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012907:Smoking / Q000009:adverse effects / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D009538:Nicotine; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase