Does the cigarette smoke exposure lead to histopathological alterations in olfactory epithelium? An electron microscopic study on a rat model (original) (raw)
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International Journal of Morphology, 2012
The objective of this study was to evaluate the histopathologic effects of systemic use of nicotine on the rat nasal mucosa. Twelve adult Sprague-Dawley rats weighing 180-220 g, were used as experimental animals. The rats were divided into Nicotine and control groups. The rats of Nicotine groups (n=6) were administered 2mg/kg Nicotine sulphate for 28 days. The rats of control group (n=6) were only administered 1,5 ml physiologic saline solution subcutaneously for 28 days. All animals were sacrified at the end of the study and nasal tissue samples were removed and prepared for histologic examination. The sections were stained with Hematoxylin and Eosin (H-E) and Periodic acid-Schiff (PAS) and Trichrome-Masson were observed under light microscope. E-cadherin immunreactivity of pseudostrafied epithelial cells of nasal mucosa was assessed by immunohistochemical staining. There were significant differences in average histopathological score between the groups treated and non-treated to nicotine. In nicotine group, degenerative change of epithelial cells and hypertrophy of goblet cells were observed. Leukocytes infiltration was observed in significant areas of connective tissue. Ecadherin expression was significantly decreased in epithelial cells of the nasal mucosa of Nicotine group.
2021
Quick Response Code Abstract: Smoking remains a global health problem because it has negative impacts either on health or economy. Smoking has various forms or types of which cigarette and waterpipe smoking are mostly prevalent. The main objectives of the present study were to investigate the histological changes resulting from exposure to cigarette and waterpipe smoking on rat trachea, and to investigate the ameliorating effects of using Ammi visnaga in reversing the adverse effects of smoking. Animal smoking model was created based on male rats that were randomly assigned in to different groups (N=8). Groups included control group, cigarette smoking group, waterpipe smoking group, cigarette smoking group treated with Ammi visnaga, and waterpipe smoking group treated with Ammi visnaga. Smoking protocol was applied for 1 month. At the end of the experiment, animals were sacrificed, trachea was isolated and placed in formalin (10%) for fixation, and tissue sections were prepared usin...
Effects of cigarette smoking on histology of trachea and lungs of albino rat
Research Opinions in Animal and Veterinary Sciences, 2013
This work was an attempt to reveal the effects of a Jordanian cigarette smoke on albino rat tissues at the cellular level. Two groups of male albino rats were exposed to the cigarette smoke for three months on a daily basis, using a special modified smoking machine. Exposure of albino rats for 3 months to cigarette smoke caused drastic histological changes in the tracheal epithelium including epithelial cells proliferation, disruption of its cilia, and presence of inclusion bodies. There was a marked thickening in the alveolar wall of lung alveoli, collapsed alveoli and blood extravasations. These changes indicate that nicotine induced changes similar to those of chronic irritation of tissue may decrease the efficiency of gaseous exchange in alveoli and predispose to neoplastic changes.
Toxicologic Pathology, 1999
In recent years, histopathologic changes have been reported in the olfactory mucosa of rodents exposed, by inhalation, to a variety of volatile chemicals. In order to better characterize these lesions, a panel of experienced pathologists reviewed microscopic lesions of the olfactory epithelium of rats reported in 10 inhalation studies conducted with 8 different chemicals. The objectives were to determine if the olfactory epithelial lesions are morphologically similar or different for the chemicals of interest, to develop and recommend appropriate diagnostic criteria and nomenclature to characterize the morphology of these olfactory lesions, and to provide specific criteria for judging the degree of severity of the olfactory changes in these studies. The results indicated that the distribution and nature of the lesions were similar in all the examined studies in which olfactory changes were observed. Recommended standardized nomenclature and diagnostic criteria and a uniform method for scoring lesion severity based on the extent of distribution and severity of tissue damage are presented.
The effect of cigarette smoke on the histopathological changes of the eustachian tube of Wistar rat
Bali Medical Journal, 2021
Background: Inflammation due to irritation of cigarette smoke causes metaplasia of the squamous epithelium of the Eustachian tube. Data on the prevalence and incidence of Eustachian tube dysfunction are still limited. The study aims to determine the effect of exposure to a stratified dose of cigarette smoke on the histopathological changes of the Eustachian tubes of Wistar rats. Method: This study was a true experimental study with post-test only control group design using Wistar rats as the subjects. We included 24 Wistar rats in the study and divided them into four groups. The number of Wistar rats in each group was 6. The control group was not exposed to cigarette smoke. The treatment group 1, 2, and 3 were each exposed to four cigarettes, eight cigarettes, twelve cigarettes per day for thirty days, respectively. We assessed the Eustachian tube histopathological changes using four parameters, namely inflammatory cells, cilia, goblet cells, and epithelium. Finally, we analyzed the data using the Kruskal-Wallis test and the Mann-Whitney test. Result: The Eustachian tube's histopathological changes occurred in inflammatory cells, cilia, goblet cells, and epithelial metaplasia. Group 1 showed grade 1 changes in all parameters assessed. Group 2 showed grade 2 changes in all parameters evaluated. Meanwhile, group 3 showed grade 3 changes in all parameters evaluated compared to other groups (p<0.05). There was a significant difference between the treatment group and the control group (p<0.05). Conclusion: Cigarette smoke with stratified doses affects the histopathological changes of the Eustachian tube.
Annual Research & Review in Biology, 2014
ABSTRACT Objectives: This work focuses on the effect of cigarette smoke exposure toxicity on the ultrastructure of selected albino rats’ cardiovascular and respiratory systems tissues from and their recovery within three months after exposure. Materials and Methods: Sixty male albino rats (Rattus norvegicus) were used in this study. Two groups, each consists of thirty rats. The first group was exposed to the cigarette smoke for three months on a daily basis, using a special modified smoking machine, while the second group (control) was left untreated. The exposure to smoking was followed by a period of three months of non-exposure to smoking as a recovery period. Following each period, the ultrastructural study was performed. Results: Cigarette smoke caused ultrastructural changes in the tracheal epithelium, heart ventricles and lung alveoli. Thin section of tracheal epithelium showed low number of cilia, a high degree of cytoplasmic vacuolization. Mitochondria aggregates in the apical portion of epithelial cells, inclusion bodies are present, and disrupted endoplasmic reticulums were also observed. The alveolar epithelium showed damaged multilamellar bodies of type II pneumocyte, together with cytoplasmic vacuolization and chromatin condensation, membrane blebs projecting from the cytoplasm, and degeneration of alveolar epithelium. The ventricular cardiomyocytes revealed mitochondria with deteriorated and partially disrupted or disappeared cristae. Also it showed areas with disrupted Z-discs. After the recovery period, those tissues showed partial recovery. Conclusion: Smoking induces ultrastructural changes in the respiratory passages and heart that affects the gaseous exchange and may predispose to cancerous changes due to accumulation of toxic and carcinogenic compounds, chromatin condensation and tissue inflammation. Cessation of exposure to cigarette smoking is important in returning most these changes to their normal ultrastructure. Keywords : Cigarette smoke; Ultrastructural change; cardiovascular system; respiratory system. - See more at: http://www.sciencedomain.org/abstract.php?iid=582&id=32&aid=5117#.VGLyLDSUcfQ
Inhalation Toxicology, 2017
Objective-Mucociliary clearance sustains a baseline functionality and an "on demand" capability to upregulate clearance upon irritant exposure involving mucus hypersecretion and accelerated ciliary beat frequency (CBF) modulated by nitric oxide (NO). This study characterized these elements as well as cellular and exogenous NO concentrations subsequent to a single exposure to tobacco smoke (TS) or e-cigarette vapor (EV) on cultured human airway epithelium. Materials and methods-Air-liquid interface (ALI) airway epithelial cultures per nonsmoking human subjects were subjected to single TS or EV exposures. Measures of ciliary function and secretion were performed and cellular and exogenous NO concentrations under control and experimental conditions were assessed. Results-Both TS and EV exposures resulted similar patterns of decline in CBF within 1 min of the completion of exposure followed by a gradual return often exceeding baseline within 1 h. Postexposure examination of exposed cultures suggested morphologic differences in secretory function relative to controls. The relative NO concentrations of TS and EV chamber air were sharply different with EV NO being only slightly elevated relative to cellular NO production. Discussion and conclusions-Epithelial remodeling and mucociliary dysfunction have been clearly associated with TS exposure. However, information contrasting epithelial structure/ function following a single acute TS or EV exposure is limited. This study demonstrates a similar pattern of epithelial response to acute TS or EV exposure. Inasmuch as NO may contribute to an Contact: Johnny L. Carson
Medical Journal of Indonesia, 2007
Asap rokok telah terbukti dapat menyebabkan berbagai gangguan pada saluran napas. Rokok kretek lebih berbahaya daripada rokok putih, karena kandungan tar, nikotin, dan karbon monoksida di dalamnya lebih tinggi. Konsumsi rokok kretek di Indonesia mencapai 88%. Efek rokok kretek terhadap saluran napas belum pernah diteliti. Tujuan penelitian ini adalah untuk mempelajari perubahan histopatologi saluran napas tikus putih galur Sprague-Dawley akibat pajanan asap rokok kretek. Penelitian dilakukan pada 20 tikus putih mulai September 2005 hingga Mei 2006. Nekropsi dilakukan setelah hari terakhir paparan asap rokok, kemudian dibuat irisan jaringan dan diproses untuk sediaan histopatologi dan diperiksa dengan mikroskop cahaya dan videomikrometer. Parameter yang diamati adalah jumlah dan tinggi epitel bersilia dan sel goblet, jumlah sel pneumosit tipe I dan II, makrofag, dan reaksi interstisial jaringan paru. Reaksi interstisial jaringan paru diamati dengan irisan semi-thin pada paru yang setelah dilakukan embedding dengan resin, dan diwarnai dengan Toluidine Blue. Hasil penelitian kami menunjukkan perubahan histopatologi yang bermakna pada saluran napas. Jumlah sel epitel pada kelompok yang terpapar asap rokok secara bermakna lebih tinggi dari kontrol (P<0.05) pada daerah sinus, bronkhus, dan bronkhiolus, sedangkan pada trakhea tidak ditemukan perbedaan bermakna (P>0.05). Jumlah sel goblet pada kelompok perlakuan juga lebih tinggi (P>0.05). Tinggi sel epitel pada kelompok perlakuan asap lebih tinggi dibandingkan kelompok kontrol, namun tidak ada perbedaan secara statistik antara tikus jantan dan betina. Terdapat perbedaan bermakna skor pneumonia interstisial (P<0.05) antara kedua kelompok. Jumlah sel pneumosit tipe II lebih banyak dibandingkan dengan sel pneumosit tipe I pada kelompok perlakuan. Berdasarkan hal-hal di atas, kami menyimpulkan bahwa paparan rokok kretek menyebabkan kelainan patologis pada saluran napas tikus. (Med J Indones 2007; 16:212-8)
Histological and biochemical effects of cigarette smoke on lungs
Acta Physiologica Hungarica, 2001
In this study, rats were made to inhale cigarette smoke in a specifically prepared container for different periods. The lung tissue samples of the subjects were examined by light microscopy, transmission electron microscopy (TEM) and scanning electron microscopy (SEM). Malonaldehyde, one of the free oxygen radicals was determined in lungs and plasma. The catalase activity level of erythrocyte and arginase levels were determined. Three groups were formed. The rats in the Ist and IInd groups were made to inhale cigarette smoke for 30 and 60 minutes a day for a total period of 3 months. Control group, the rats in the IIIrd group (controls) were made to inhale clean air during the same periods. An increase in the number of macrophages was observed in the pulmonary tissue of the exposed groups. Especially in the group that inhaled the smoke for long periods, the number of macrophages and the inclusion bodies contained in them increased. These differences could easily be observed in TEM studies. In the light microscopy and SEM observations, it arouse attention that the alveolar macrophages occurred as sets and their activation increased. Depending on the length of the exposure to cigarette smoke, an increase in the number of macrophages was observed. Statistically significant increases were determined in the malonaldehyde levels of pulmonary tissue and plasma when compared to the control group. Besides significant increases were found in the catalase activity levels of erythrocytes in the experimental groups.