دورية أكاديمية
In vivo hydroquinone exposure causes tracheal hyperresponsiveness due to TNF secretion by epithelial cells.
| العنوان: | In vivo hydroquinone exposure causes tracheal hyperresponsiveness due to TNF secretion by epithelial cells. |
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| المؤلفون: | Shimada AL; Laboratory of Experimental Toxicology, Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, Brazil., Lino-Dos-Santos-Franco A, Bolonheis SM, Nakasato A, Damazo AS, Tavares-de-Lima W, Farsky SH |
| المصدر: | Toxicology letters [Toxicol Lett] 2012 May 20; Vol. 211 (1), pp. 10-7. Date of Electronic Publication: 2012 Mar 05. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier Country of Publication: Netherlands NLM ID: 7709027 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-3169 (Electronic) Linking ISSN: 03784274 NLM ISO Abbreviation: Toxicol Lett Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Amsterdam : Elsevier Original Publication: Amsterdam, Elsevier/North Holland. |
| مواضيع طبية MeSH: | Hydroquinones/*adverse effects , Respiratory Mucosa/*drug effects , Trachea/*drug effects , Tumor Necrosis Factor-alpha/*metabolism, Animals ; Chlorpromazine/pharmacology ; Dose-Response Relationship, Drug ; Male ; Mast Cells/drug effects ; Methacholine Chloride/pharmacology ; Mice ; Muscle Contraction/drug effects ; Respiratory Mucosa/metabolism |
| مستخلص: | Hydroquinone (HQ) is the main oxidative substance in cigarette smoke and a toxic product of benzene biotransformation. Although the respiratory tract is an inlet pathway of HQ exposure, its effect on airway muscle responsiveness has not been assessed. We thus investigated the effects of low dose in vivo HQ-exposure on tracheal responsiveness to a muscarinic receptor agonist. Male Swiss mice were exposed to aerosolised 5% ethanol/saline solution (HQ vehicle; control) or 0.04 ppm HQ (1h/day for 5 days) and tracheal rings were collected 1h after the last exposure. HQ exposure caused tracheal hyperresponsiveness to methacholine (MCh), which was abolished by mechanical removal of the epithelium. This hyperresponsiveness was not dependent on neutrophil infiltration, but on tumour necrosis factor (TNF) secretion by epithelial cells. This conclusion was based on the following data: (1) trachea from HQ-exposed mice presented a higher amount of TNF, which was abrogated following removal of the epithelium; (2) the trachea hyperresponsiveness and TNF levels were attenuated by in vivo chlorpromazine (CPZ) treatment, an inhibitor of TNF synthesis. The involvement of HQ-induced TNF secretion in trachea mast cell degranulation was also demonstrated by the partial reversion of tracheal hyperresponsiveness in sodium cromoglicate-treated animals, and the in vivo HQ-exposure-induced degranulation of trachea connective tissue and mucosal mast cells, which was reversed by CPZ treatment. Our data show that in vivo HQ exposure indirectly exacerbates the parasympathetic-induced contraction of airway smooth muscle cells, mediated by TNF secreted by tracheal epithelial cells, clearly showing the link between environmental HQ exposure and the reactivity of airways. (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.) |
| المشرفين على المادة: | 0 (Hydroquinones) 0 (Tumor Necrosis Factor-alpha) 0W5ETF9M2K (Methacholine Chloride) U42B7VYA4P (Chlorpromazine) XV74C1N1AE (hydroquinone) |
| تواريخ الأحداث: | Date Created: 20120315 Date Completed: 20120629 Latest Revision: 20181201 |
| رمز التحديث: | 20221213 |
| DOI: | 10.1016/j.toxlet.2012.02.016 |
| PMID: | 22414385 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder | تدمد: | 1879-3169 |
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| DOI: | 10.1016/j.toxlet.2012.02.016 |