کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9889983 | 1539995 | 2005 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Acetaminophen decreases intracellular glutathione levels and modulates cytokine production in human alveolar macrophages and type II pneumocytes in vitro
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
troleandomycinPGHSDDTCTAOIL-6DMEMFBSIL-8CyPAPAPGSHPEXdeoxyribonuclease3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide - 3- [4،5-dimethylthiazol-2-yl] -2،5-diphenyltetrazolium bromideDNAse - DNAaseDulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده DulbeccoMTT - MTTAsthma - آسمPotassium ethyl xanthate - اتیل کاسنگات پتاسیمAcetaminophen - استامینوفن interleukin 6 - اینترلوکین 6Interleukin 8 - اینترلوکین 8tumor necrosis factor-α - تومور نکروز عامل αDiethyldithiocarbamic acid - دی اتیل دی اتیل کربام اسیدfetal bovine serum - سرم جنین گاوLung cells - سلولهای ریهCytochrome P450 - سیتوکروم پی۴۵۰Cytokines - سیتوکین هاTNF-α - فاکتور نکروز توموری آلفاParacetamol - پاراستامولreduced glutathione - کاهش گلوتاتیونGlutathione - گلوتاتیون
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Acetaminophen decreases intracellular glutathione levels and modulates cytokine production in human alveolar macrophages and type II pneumocytes in vitro Acetaminophen decreases intracellular glutathione levels and modulates cytokine production in human alveolar macrophages and type II pneumocytes in vitro](/preview/png/9889983.png)
چکیده انگلیسی
Recent epidemiological observations suggest that acetaminophen (paracetamol) may contribute to asthma morbidity. Impaired endogenous antioxidant defences may have a role in the pathogenesis of a number of inflammatory pulmonary diseases, including asthma. We studied the effect of acetaminophen on the intracellular level of reduced glutathione (GSH) with and without inhibitors of cytochrome P450 or prostaglandin H synthetase, and TNF-α, IL-6 and IL-8 protein production in human alveolar macrophages and type II pneumocytes in vitro. Following a 20 h incubation with acetaminophen, cytotoxicity was apparent from â¥5 and â¥10 mM in macrophages and type II pneumocytes, respectively. A time- and concentration-dependent decrease of intracellular GSH occurred after acetaminophen (0.05-1 mM) exposure (1-4 h) in pulmonary macrophages (up to 53%) and type II pneumocytes (up to 34%). Diethyldithiocarbamic acid, potassium ethyl xanthate, and indomethacin decreased significantly acetaminophen-induced GSH depletion in the two cell types tested, suggesting the involvement of cytochrome P450 (mainly CYP2E1) and/or prostaglandin H synthetase. In macrophages, acetaminophen decreased the secretion of TNF-α (at 4 and 24 h, concentration-related) and IL-6 (at 24 h, at 0.1 mM), and did not affect significantly IL-8 production. These in vitro observations demonstrate that clinically relevant concentrations of acetaminophen decreased: (i) intracellular GSH in human pulmonary macrophages and type II pneumocytes and (ii) the secretion of TNF-α and possibly IL-6 by human pulmonary macrophages. These findings provide experimental plausibility to the challenging observations that frequent use of APAP may be a risk factor for asthma morbidity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 37, Issue 8, August 2005, Pages 1727-1737
Journal: The International Journal of Biochemistry & Cell Biology - Volume 37, Issue 8, August 2005, Pages 1727-1737
نویسندگان
Svetlana Dimova, Peter H.M. Hoet, David Dinsdale, Benoit Nemery,