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过氧化物酶基因在支气管上皮细胞暴露于柴油机排气颗粒中的表达模式。

Expression patterns of peroxiredoxin genes in bronchial epithelial cells exposed to diesel exhaust particles.

机构信息

Laboratory of Experimental Air Pollution (LIM05), Department of Pathology, School of Medicine, University of São Paulo, FMUSP- Av. Dr. Arnaldo 455, 1°floor, room 1150, São Paulo, SP 01246-903, Brazil; PROSCED - Consulting, Training and Development, Rua Alto Belo, 742, room 01, São Paulo, SP 03478-040, Brazil.

Genetic and Evolution Department, Federal University of São Carlos, UFSCar- Av. Washington Luiz Km 235, São Carlos, SP 13565-905, Brazil.

出版信息

Exp Mol Pathol. 2021 Jun;120:104641. doi: 10.1016/j.yexmp.2021.104641. Epub 2021 Apr 23.

DOI:10.1016/j.yexmp.2021.104641
PMID:33901418
Abstract

Several mechanisms have been suggested to explain the adverse effects of air pollutants on airway cells. One such explanation is the presence of high concentrations of oxidants and pro-oxidants in environmental pollutants. All animal and plant cells have developed several mechanisms to prevent damage by oxidative molecules. Among these, the peroxiredoxins (PRDXs) are of interest due to a high reactivity with reactive oxygen species (ROS) through the functioning of the thioredoxin/thioredoxin reductase system. This study aimed to verify the gene expression patterns of the PRDX family in bronchial epithelial airway cells (BEAS-2B) cells exposed to diesel exhaust particles (DEPs) at a concentration of 15 μg/mL for 1 or 2 h because this it is a major component of particulate matter in the atmosphere. There was a significant decrease in mRNA fold changes of PRDX2 (0.43 ± 0.34; *p = 0.0220), PRDX5 (0.43 ± 0.34; *p = 0.0220), and PRDX6 (0.33 ± 0.25; *p = 0.0069) after 1 h of exposure to DEPs. The reduction in mRNA levels may consequently lead to a decrease in the levels of PRDX proteins, increasing oxidative stress in bronchial epithelial cells BEAS-2B and thus, negatively affecting cellular functions.

摘要

已有多种机制被提出用以解释空气污染物对气道细胞的有害影响。其中一种解释是环境污染物中存在高浓度的氧化剂和促氧化剂。所有动植物细胞都发展了几种机制来防止氧化分子造成损伤。在这些机制中,过氧化物酶(PRDXs)由于通过硫氧还蛋白/硫氧还蛋白还原酶系统的作用与活性氧(ROS)具有高反应性而引起关注。本研究旨在验证在浓度为 15μg/mL 的柴油废气颗粒(DEPs)下暴露 1 或 2 小时后,支气管上皮气道细胞(BEAS-2B)细胞中 PRDX 家族的基因表达模式,因为它是大气颗粒物的主要成分之一。暴露于 DEPs 1 小时后,PRDX2(0.43±0.34;*p=0.0220)、PRDX5(0.43±0.34;*p=0.0220)和 PRDX6(0.33±0.25;*p=0.0069)的 mRNA 折叠变化显著下降。mRNA 水平的降低可能导致 PRDX 蛋白水平降低,从而增加支气管上皮细胞 BEAS-2B 的氧化应激,并因此对细胞功能产生负面影响。

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