Comparative study of PM2.5 - and PM10 - induced oxidative stress in rat lung epithelial cells.
Accurate estimation of the exposure-response relationship between ambient urban particulate matters (PM) and public health is important for regulatory perspective of ambient urban particulate matters (PM). Ambient PM contains various transition metals and organic compounds. PM10 (aerodynamic diameter less than 10 micro m) is known to induce diverse diseases such as chronic cough, bronchitis, chest illness, etc. However, recent evaluation of PM2.5 (aerodynamic diameter less than 2.5 micro m) against health outcomes has suggested that the fine particles may be more closely associated with adverse respiratory health effects than particles of larger size. This study was performed to evaluate PM2.5-induced oxidative stress in rat lung epithelial cell in order to provide basic data for the risk assessment of PM2.5. PM2.5 showed higher cytotoxicity than PM10. Also, PM 2.5 induced more malondialdehyde (MDA) formation than PM10. In Hoechst 33258 dye staining and DNA fragmentation assay, apopotic changes were clearly detected in PM2.5 treated cells in compared to PM10. Expression of catalase mRNA was increased by PM2.5 rather than PM10. PM2.5 induced higher Mth1 mRNA than PM10. In pBR322 DNA treated with PM2.5, production of single strand breakage of DNA was higher than that of PM10. In Western blot analysis, PM2.5 induced more Nrf-2 protein, associated with diverse transcriptional and anti-oxidative stress enzymes, compared to PM10. Our data suggest that PM2.5 rather than PM10 may be responsible for PM-induced toxicity. Additional efforts are needed to establish the environmental standard of PM2.5.
Choi
Jin-Hyuk
JH
Laboratory of Toxicology, College of Veterinary Medicine, and School of Agricultural Biotechnology, Seoul National University, Seoul 151-742, Korea.
Kim
Jun-Sung
JS
Kim
Young-Chul
YC
Kim
Yoon-Shin
YS
Chung
Nam-Hyun
NH
Cho
Myung-Haing
MH
D000393:Air Pollutants / Q000737:chemistry / Q000633:toxicity*; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001562:Benzimidazoles / Q000378:metabolism; D015153:Blotting, Western; D002460:Cell Line; D002470:Cell Survival / Q000502:physiology; D053938:DNA Fragmentation / Q000502:physiology; D045643:DNA Repair Enzymes / Q000235:genetics / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D004847:Epithelial Cells / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D005562:Formazans / Q000378:metabolism; D051268:GA-Binding Protein Transcription Factor; D008054:Lipid Peroxides / Q000378:metabolism; D008171:Lung Diseases / Q000139:chemically induced* / Q000201:enzymology / Q000473:pathology; D018384:Oxidative Stress / Q000502:physiology*; D012333:RNA, Messenger / Q000737:chemistry / Q000235:genetics; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013778:Tetrazolium Salts / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism
D000393:Air Pollutants; D001562:Benzimidazoles; D004268:DNA-Binding Proteins; D005562:Formazans; D051268:GA-Binding Protein Transcription Factor; D008054:Lipid Peroxides; D012333:RNA, Messenger; D013778:Tetrazolium Salts; D014157:Transcription Factors; C447680:hoechst 32258; C079782:MTT formazan; D045643:DNA Repair Enzymes