NDLI: Organic extracts of urban air pollution particulate matter (PM2.5)-induced genotoxicity and oxidative stress in human lung bronchial epithelial cells (BEAS-2B cells).

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Oh, Seung Min Kim, Ha Ryong Park, Yong Joo Lee, Soo Yeun Chung, Kyu Hyuck
Spatial Coverage	Korea
Description	Author Affiliation: Oh SM ( Hoseo Toxicological Research Center, Hoseo University, 165, Sechul-ri, Baebang-myun, Asan, Chungnam, 336-795, Republic of Korea.)
Abstract	Traffic is a major source of particulate matter (PM), and ultrafine particulates and traffic intensity probably contribute significantly to PM-related health effects. As a strong relationship between air pollution and motor vehicle-originated pollutants has been shown to exist, air pollution genotoxicity studies of urban cities are steadily increasing. In Korea, the death rate caused by lung cancer is the most rapidly increased cancer death rate in the past 10 years. In this study, genotoxicity of PM2.5 (<2.5µm in aerodynamic diameter particles) collected from the traffic area in Suwon City, Korea, was studied using cultured human lung bronchial epithelial cells (BEAS-2B) as a model system for the potential inhalation health effects. Organic extract of PM2.5 (CE) generated significant DNA breakage and micronucleus formation in a dose-dependent manner (1µg/cm(3)-50µg/cm(3)). In the acid-base-neutral fractionation of PM2.5, neutral samples including the aliphatic (F3), aromatic (F4) and slightly polar (F5) fractions generated significant DNA breakage and micronucleus formation. These genotoxic effects were significantly blocked by scavenging agents [superoxide dismutase (SOD), sodium selenite (SS), mannitol (M), catalase (CAT)]. In addition, in the modified Comet assay using endonucleases (FPG and ENDOIII), CE and its fractions (F3, F4, and F5) increased DNA breakage compared with control groups, indicating that CE and fractions of PM2.5 induced oxidative DNA damage. These results clearly suggest that PM2.5 collected in the Suwon traffic area has genotoxic effects and that reactive oxygen species may play a distinct role in these effects. In addition, aliphatic/chlorinated hydrocarbons, PAH/alkylderivatives, and nitro-PAH/ketones/quinones may be important causative agents of the genotoxic effects.
File Format	HTM / HTML
ISSN	13835718
e-ISSN	18793592
Journal	Mutation Research/Genetic Toxicology and Environmental Mutagenesis
Issue Number	2
Volume Number	723
Language	English
Publisher	Elsevier
Publisher Date	2011-08-16
Publisher Place	Netherlands
Access Restriction	Open
Subject Keyword	Cell Line Research Support, Non-u.s. Gov't Discipline Genetics Reactive Oxygen Species Oxidative Stress Toxicity Bronchi Discipline Biochemistry Respiratory Mucosa Drug Effects Dna Damage Air Pollutants Mutagenicity Tests Particulate Matter Korea
Content Type	Text
Resource Type	Article
Subject	Genetics Health, Toxicology and Mutagenesis

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