亚急性聚乙烯微塑料吸入暴露通过炎症和氧化应激诱导wistar大鼠肺毒性。

Q1 Environmental Science
Toxicology Reports Pub Date : 2025-06-10 eCollection Date: 2025-06-01 DOI:10.1016/j.toxrep.2025.102067
Athaya Rahmanardi Muhammad, Muhammad Reva Aditya, Bayu Lestari, Hikmawan Wahyu Sulistomo
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引用次数: 0

摘要

塑料废物,特别是聚乙烯(PE)塑料袋和塑料瓶,在降解为微塑料时,会造成严重的环境问题和健康风险。最近大气中的微塑料污染增加了吸入量,因此有必要研究其对肺部的毒性。然而,PE微塑料的吸入毒性尚不清楚。本研究采用Wistar大鼠,分为对照组和PE组。PE组吸入PE微塑料28天,日剂量为15 mg/m3。与对照组相比,PE组炎性渗出物、肺泡增厚、NF-κB等炎症标志物明显升高。PE组MDA升高,SOD降低,提示发生了氧化应激。这些结果提示,亚急性PE微塑料吸入可能通过NF-κB途径参与氧化应激引起的炎症发病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sub-acute polyethylene microplastic inhalation exposure induced pulmonary toxicity in wistar rats through inflammation and oxidative stress.

Plastic waste, particularly polyethylene (PE) plastic bags and bottles, poses a significant environmental problem and health risk when degraded into microplastics. Recent atmospheric microplastic pollution increases inhalation exposure, necessitating a study on toxicity in the lungs. However, the inhalation toxicology of PE microplastics is poorly understood. This study used Wistar rats that are divided into control and PE group. The PE groups were exposed to PE microplastic through inhalation for 28 days with the daily dose of 15 mg/m3. Inflammatory marker such as Inflammatory exudate, Alveolar thickening, and NF-κB were in PE group increased significantly compared to control group. the increment of MDA and decrement of SOD in PE group revealed the oxidative stress occurred. These results suggest that sub-acute PE microplastic inhalation may contribute to inflammation pathogenesis via the NF-κB pathway as a result of oxidative stress.

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来源期刊
Toxicology Reports
Toxicology Reports Environmental Science-Health, Toxicology and Mutagenesis
CiteScore
7.60
自引率
0.00%
发文量
228
审稿时长
11 weeks
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