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出生后接触臭氧和超细颗粒会破坏气管支气管气道的生长。

Disruption of tracheobronchial airway growth following postnatal exposure to ozone and ultrafine particles.

机构信息

Department of Mechanical and Aerospace Engineering, University of California, Davis, CA 95616, USA.

出版信息

Inhal Toxicol. 2011 Aug;23(9):520-31. doi: 10.3109/08958378.2011.591447. Epub 2011 Jul 22.

Abstract

This study examined airway structure changes in adult rats after a long recovery period due to sub-chronic juvenile exposure to ozone and ultrafine particles that have a high organic fraction. Neonatal male Sprague-Dawley rats were exposed during lung development to 3 cycles of 0.5 ppm ozone from postnatal day 7 through 25. Two different exposure patterns were used: 5-day exposure per week (Ozone52) or 2-day exposure per week (Ozone25) with or without co-exposure to ultrafine particles (OPFP5252, OPFP5225). Airway architecture was evaluated at 81 days of age, after 56 days of continued development beyond the exposure period in filtered air (FA). By analyzing CT images from lung airway casts, we determined airway diameter, length, branching angle, and rotation angle for most conducting airways. Compared with the FA control group, the Ozone52 group showed significant decreases in airway diameter in generations larger than 10 especially in the right diaphragmatic lobe and in airway length in distal generations, while changes in airway structure due to the Ozone25 exposure were not appreciable. Interaction effects of ozone and ultrafine particle exposures were not significant. These results suggest that airway alterations due to postnatal ozone exposure are not limited to the distal region but occur extensively from the middle to distal conducting airways. Further, alterations due to early ozone exposure do not recover nearly 2 months after exposure has ceased demonstrating a persistent airway structural change following an early life exposure to ozone.

摘要

本研究考察了成年大鼠在经历亚慢性幼年臭氧和具有高有机成分的超细颗粒暴露后长时间恢复期内气道结构的变化。新生雄性 Sprague-Dawley 大鼠在肺发育过程中暴露于 0.5 ppm 臭氧,从出生后第 7 天至第 25 天,每周进行 3 个循环。使用了两种不同的暴露模式:每周 5 天暴露(Ozone52)或每周 2 天暴露(Ozone25),同时或不与超细颗粒(OPFP5252、OPFP5225)共同暴露。在暴露期后继续在过滤空气中发育 56 天后,在 81 天大时评估气道结构。通过分析来自肺气道铸型的 CT 图像,我们确定了大多数传导气道的气道直径、长度、分支角度和旋转角度。与 FA 对照组相比,Ozone52 组在第 10 代以上的气道直径明显减小,尤其是右膈叶,在远端气道的气道长度也明显减小,而 Ozone25 暴露引起的气道结构变化不明显。臭氧和超细颗粒暴露的相互作用效应不显著。这些结果表明,出生后臭氧暴露引起的气道改变不仅限于远端区域,而且从中间到远端传导气道广泛发生。此外,早期臭氧暴露引起的改变在暴露停止后近 2 个月几乎没有恢复,表明早期生命暴露于臭氧后会持续发生气道结构变化。

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