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气管内吸入三氧化二砷对大鼠肺部的急性毒性。

Acute toxicity of intratracheal arsenic trioxide instillation in rat lungs.

机构信息

Chinese People's Liberation Army Center of Disease Control and Prevention, Beijing, China.

出版信息

J Appl Toxicol. 2019 Nov;39(11):1578-1585. doi: 10.1002/jat.3841. Epub 2019 Jul 18.

Abstract

This study investigated the acute toxicity of different concentrations of arsenic trioxide (As O ; ATO) on rat lungs. In total, 160 Wistar rats were randomly divided into the control, low-, medium- and high-dose groups, which were exposed to 0, 0.16, 1.60 and 16 μg/kg of ATO by intratracheal instillation, respectively. Samples were collected at 6, 12, 24, 48 and 72 hours after exposure and the dynamic changes indicative of acute lung toxicity were monitored. Compared with the control group, the exposure groups exhibited significant changes such as increased lung water content ratio and protein concentration in the bronchoalveolar lavage fluid, pulmonary interstitial thickening, cell membrane edema, increased inflammatory factor concentration, JNK and P38 were significantly activated, and the degree of phosphorylation was increased. Furthermore, all the changes in the exposure groups were exposure concentration-dependent. ATO respiratory tract exposure can cause restrictive ventilatory disturbance in rats, and the degree of injury is exposure concentration-dependent.

摘要

本研究考察了不同浓度三氧化二砷(As O ;ATO)对大鼠肺部的急性毒性。将 160 只 Wistar 大鼠随机分为对照组、低剂量组、中剂量组和高剂量组,分别通过气管内滴注暴露于 0、0.16、1.60 和 16μg/kg 的 ATO。暴露后 6、12、24、48 和 72 小时采集样本,监测提示急性肺毒性的动态变化。与对照组相比,暴露组的肺水含量比和支气管肺泡灌洗液中的蛋白浓度、肺间质增厚、细胞膜水肿、炎症因子浓度增加、JNK 和 P38 显著激活,磷酸化程度增加。此外,暴露组的所有变化均呈暴露浓度依赖性。ATO 呼吸道暴露可导致大鼠限制性通气障碍,损伤程度呈暴露浓度依赖性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca33/6852324/8b72df4cf041/JAT-39-1578-g001.jpg

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