Department of Environmental Health Science, School of Public Health, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Am J Respir Cell Mol Biol. 2012 May;46(5):599-606. doi: 10.1165/rcmb.2011-0196OC. Epub 2011 Dec 8.
We assessed the safety and efficacy of combined intravenous and aerosolized antioxidant administration to attenuate chlorine gas-induced airway alterations when administered after exposure. Adult male Sprague-Dawley rats were exposed to air or 400 parts per million (ppm) chlorine (a concentration likely to be encountered in the vicinity of industrial accidents) in environmental chambers for 30 minutes, and returned to room air, and they then received a single intravenous injection of ascorbic acid and deferoxamine or saline. At 1 hour and 15 hours after chlorine exposure, the rats were treated with aerosolized ascorbate and deferoxamine or vehicle. Lung antioxidant profiles, plasma ascorbate concentrations, airway morphology, and airway reactivity were evaluated at 24 hours and 7 days after chlorine exposure. At 24 hours after exposure, chlorine-exposed rats had significantly lower pulmonary ascorbate and reduced glutathione concentrations. Treatment with antioxidants restored depleted ascorbate in lungs and plasma. At 7 days after exposure, in chlorine-exposed, vehicle-treated rats, the thickness of the proximal airways was 60% greater than in control rats, with twice the amount of mucosubstances. Airway resistance in response to methacholine challenge was also significantly elevated. Combined treatment with intravenous and aerosolized antioxidants restored airway morphology, the amount of airway mucosubstances, and airway reactivity to control levels by 7 days after chlorine exposure. Our results demonstrate for the first time, to the best of our knowledge, that severe injury to major airways in rats exposed to chlorine, as characterized by epithelial hyperplasia, mucus accumulation, and airway hyperreactivity, can be reversed in a safe and efficacious manner by the post-exposure administration of ascorbate and deferoxamine.
我们评估了联合静脉和雾化抗氧化剂给药的安全性和疗效,以减轻氯气暴露后给药时引起的气道改变。成年雄性 Sprague-Dawley 大鼠在环境室中暴露于空气或 400ppm 氯气(在工业事故附近可能遇到的浓度)30 分钟,然后返回室内空气,然后接受单次静脉注射抗坏血酸和去铁胺或生理盐水。在氯气暴露后 1 小时和 15 小时,用雾化抗坏血酸和去铁胺或载体处理大鼠。在氯气暴露后 24 小时和 7 天评估肺抗氧化剂谱、血浆抗坏血酸浓度、气道形态和气道反应性。暴露后 24 小时,氯气暴露大鼠肺组织和血浆中的抗坏血酸和还原型谷胱甘肽浓度明显降低。抗氧化剂治疗恢复了肺和血浆中耗尽的抗坏血酸。暴露后 7 天,在氯气暴露、载体处理的大鼠中,近端气道的厚度比对照大鼠增加了 60%,粘蛋白物质的含量增加了一倍。对乙酰甲胆碱挑战的气道阻力也显著升高。联合静脉和雾化抗氧化剂治疗在氯气暴露后 7 天内使气道形态、气道粘蛋白物质的含量和气道反应性恢复到对照水平。我们的研究结果首次表明,在我们所知的范围内,暴露于氯气的大鼠主要气道严重损伤,表现为上皮增生、粘液积聚和气道高反应性,可通过暴露后给予抗坏血酸和去铁胺安全有效地逆转。