|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|5561984||1403401||2018||7 صفحه PDF||سفارش دهید||دانلود کنید|
- Cl2 causes a concentration-dependent inflammatory response and lung injury.
- 8-Isoprostane formation is through direct oxidation of arachidonic acid by Cl2.
- 8-Isoprostane represents a promising high sensitivity biomarker for Cl2-induced ALI.
Inhalation of chlorine (Cl2) may cause oxidative acute lung injury (ALI) characterized by pulmonary edema, pneumonitis, and hyperreactive airways. The aim of the study was to identify possible biomarkers for Cl2-induced ALI.Female BALB/c mice were exposed to Cl2 for 15Â min using two protocols 1) concentration-dependent response (25-200Â ppm) and 2) time-kinetics (2h-14Â days post-exposure).Exposure to 50-200Â ppm Cl2 caused a concentration-dependent inflammatory response with increased expression of IL-1Î², IL-6 and CXCL1/KC in bronchoalveolar lavage fluid 2-6Â h after exposure which was followed by increased lung permeability and a neutrophilic inflammation 12-24Â h post-exposure. The early inflammatory cytokine response was associated with a clear but transient increase of 8-isoprostane, a biomarker for oxidative stress, with its maximum at 2Â h after exposure. An increase of 8-isoprostane could also be detected in serum 2Â h after exposure to 200Â ppm Cl2, which was followed by increased levels of IL-6 and CXCL1/KC and signs of increased fibrinogen and PAI-1. Melphalan, a non-oxidizing mustard gas analog, did not increase the 8-isoprostane levels, indicating that 8-isoprostane is induced in airways through direct oxidation by Cl2. We conclude that 8-isoprostane represents an early biomarker for oxidative stress in airways and in the blood circulation following Cl2-exposure.
Journal: Toxicology Letters - Volume 282, 5 January 2018, Pages 1-7