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Environ Sci Pollut Res Int. 2018 Aug;25(23):22408-22419. doi: 10.1007/s11356-017-0430-3. Epub 2017 Nov 2.

Oxidative stress and cell cycle arrest induced by short-term exposure to dustfall PM2.5 in A549 cells.

Author information

1
Department of Clinical Laboratory, Southwest Medical University, Luzhou, Sichuan Province, 646000, China.
2
School of Environmental Resource and Engineering, Southwest University of Science and Technology, Mianyang, Sichuan Province, 621003, China.
3
Medical Laboratory, Sichuan Mianyang 404 hospital, No.2 Affiliated Hospital of North Sichuan Medical College, Mianyang, Sichuan Province, 621000, China.
4
Department of Clinical Laboratory, Southwest Medical University, Luzhou, Sichuan Province, 646000, China. jianjundeng0801@163.com.
5
Medical Laboratory, Sichuan Mianyang 404 hospital, No.2 Affiliated Hospital of North Sichuan Medical College, Mianyang, Sichuan Province, 621000, China. jianjundeng0801@163.com.

Abstract

It was reported that in vitro short-term exposure to PM2.5 caused different lung diseases through inflammatory response, immune toxicity, oxidative stress, and genetic mutations. However, the complex molecular biological mechanism for its toxicity had not been fully elucidated. Therefore, the present study investigated the cytotoxicity, oxidative damage, mitochondria damage, apoptosis, and cell cycle arrest of NX and QH PM2.5 in A549 cells. Further, cell cycle arrest-related gene levels in PM2.5-induced A549 cells were also detected. Our results suggested that PM2.5 reduced the cell viability in A549 cells. Simultaneously, excessive ROS decreased MMP levels and damaged mitochondrial membrane integrity and induced mitochondrial oxidative damage through the oxygen-dependent killer route, resulting in mitochondrial damage and cell apoptosis. Besides, the results also showed that PM2.5 induced A549 cell cycle alteration in G2/M phase after co-culture for 24 h. G2/M phase arrest was induced by upregulation of p53 and p21 and downregulation of CDK1 mRNA expression. In addition, lncRNA Sox2ot might play an important role as the specific oncogenes and it participated in G2/M phase arrest by regulating the expression of EZH2.

KEYWORDS:

A549 cells; Cell cycle arrest; Dustfall PM2.5; Oxidative stress; Short-term exposure

PMID:
29098582
DOI:
10.1007/s11356-017-0430-3
[Indexed for MEDLINE]

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