实验动物科学 ›› 2024, Vol. 41 ›› Issue (6): 34-40.DOI: 10. 3969 / j. issn. 1006-6179. 2024. 06. 007

• 论著 • 上一篇    下一篇

工业废渣铝灰提取物对大鼠呼吸系统的毒性

  

  1. ( 1. 甘肃省分析测试中心,兰州 730000)  ( 2. 甘肃省固体废物与化学品中心,兰州 730000)
    ( 3. 甘肃省中医药大学,兰州 730000)
  • 收稿日期:2023-08-09 出版日期:2024-12-28 发布日期:2025-01-15
  • 通讯作者: 孙缨泽( 1987—) ,男,助理研究员,研究方向为环境评价与检测分析,E-mail:1064194558@ qq. com。
  • 作者简介:共同第一作者 刘 兰( 1965—) ,女,正高级工程师,研究方向为环境评价与检测分析,实验动物管理,E-mail:1500868827@ qq. com。 闵 哲( 1983—) ,男,助理研究员,研究方向为实验动物信息系统管理,E-mail: 119237093@ qq. com。
  • 基金资助:
    中央引导地方科技发展专项(YDZX20216200004349)

Industrial Waste Residue Study on Respiratory System Toxicity Effect of Aluminum Ash Extracts in Rats

  1. ( 1. Gansu Province Analysis and Testing Center, Lanzhou 730000,China)
    ( 2. Gansu Solid Waste and Chemical Center, Lanzhou 730000,China)
    ( 3. Gansu University of Chinese Medicine, Lanzhou 730000,China)
  • Received:2023-08-09 Online:2024-12-28 Published:2025-01-15

摘要:

目的 通过铝灰渣提取物(AAE) ,构建大鼠肺部吸入模型,检测 AAE 对肺部的影响。 方法 针对 AAE 的不同剂量和染毒时间,检测肺部的生理生化特征,以及肺部的炎症程度。 结果 雾化吸入 AAE 后,即便低剂量的吸入也可以在短时间内导致大鼠的肺损伤,并且损伤程度与吸入剂量和时间呈显著正相关。 实验结果进一步表明AAE 的吸入所导致的肺部损伤,主要在于 AAE 激活了肺部中性粒细胞,进而促使其释放更多的促炎因子 TNF-α、IL-6、IL-1β 和炎症介质髓过氧化物酶(MPO) 、丙二醛(MDA) 。 结论 本研究结果揭示了工业固体废物铝灰存在对呼吸道损伤的可能和潜在机制,为促进制铝企业工业废弃物的规范处理提供参考。

关键词:

Abstract: Objective Aluminum ash residue extract (AAE) and constructed a rat lung inhalation model to test the effects of AAE on the lungs. Method The physiological and biochemical characteristics of the lungs, as well as the degree of inflammation in the lungs, were examined for different doses and dyeing times of AAE. Result The experimental result showed that nebulized inhalation of AAE could lead to lung injury in rats within a short period of time, even at low doses, and the degree of injury was significantly positively correlated with the inhalation dose and time. The experimental result further indicated that the lung injury caused by the inhalation of AAE was mainly due to the activation of lung neutrophils by AAE, which promoted the release of more pro-inflammatory factors TNF-α, IL-6, IL-1β, and inflammatory mediators MPO and MDA. Conclusion The result of this study reveal the possibility and potential mechanism of industrial solid waste aluminum ash to respiratory tract injury, and provide a reference for promoting the standardized treatment of industrial waste in aluminum manufacturing enterprises.

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