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Diffusion flame-derived fine particulate matters doped with iron caused genotoxicity in B6C3F1 mice
Park, Jin Hong,Han, Kyu Tae,Eu, Kook-Jong,Kim, Jun-Sung,Chung, Kyu Hyuk,Park, Bio,Yang, Go Su,Lee, Kee-Ho,Cho, Myung-Haing PRINCETON SCIENTIFIC PUBLISHING CO 2005 TOXICOLOGY AND INDUSTRIAL HEALTH Vol.21 No.3-4
<P>Potential genotoxic effects of diffusion flame-derived particulate matters (PMs), known to cause various adverse health problems, doped with iron, one of the representative heavy metals frequently found in the atmosphere, were examined. B6C3F1 mice were exposed to PMs [chamber 1 (low), 100; chamber 2 (middle), 200; and chamber 3 (high), 400 microg/m3] for 6 h/day, 5 days/week for one, two and four weeks in 1.5 m3 whole-body inhalation chambers. Our diffusion flame system produced 94.8 and 5.2% fine PM2.5 and PM10, respectively, with 89% of PM2.5 sized between 0.1 and 0.2 microm. Two cytogenetic endpoints were investigated through chromosomal aberration and supravital micronucleus (SMN) assays. Frequencies of cells with chromosome aberration (%) were observed in time- and concentration-dependent manners except in one-week exposure group, as also observed in SMN study. Generally, noniron flame induced less chromosome aberration than iron-doped flame, an indication that iron particles could potentiate urban PM toxicity. The above results indicate our diffusion flame system generated genotoxic fine PMs, whose effects were potentiated by organometallic particles such as iron. Our system can provide reliable PM models for studying the toxicity of urban fine PMs applicable for risk assessment.</P>
Min Young Kim,Kyung Suk Song,Gun Ho Park,Hyun Woo Kim,Jin Hong Park,Jun Sung Kim,Hwa Jin,Kook Jong Eu,Hyun Sun Cho,Gami Kang,Chanhee Chae,Yoon Shin Kim,Young Chul Kim,Hae Yeong Kim,George Beck,Nancy C 한국독성학회 2004 Toxicological Research Vol.20 No.1
Changes in cell cycle control in the lungs and liver of the B6C3F1 mice (20 males per each group) exposed to ozone (0.5 ppm), 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK, 1.0 mg/kg), and dibutyl phthalate (DBP, 5,000 ppm) after 52 weeks were examined through Western, Northern blot, and immunohistochemistry based on alterations in protein expression levels of G1/S checkpoints (cyclin D1, cyclin E, and PCNA), G2/M checkpoints (cyclin B1, cyclin G, and cyclin A), negative regulators (p53, p21, GADD45, and p27), and positive regulator (mdm2). Expression levels of cyclins D1, E, G, PCNA, mutant p53, and mdm2 proteins were higher in the lungs<br/> and livers treated with combination of toxicants than in those treated with ozone only. Expression levels of the wild-type and mutant p53, p21, GADD45, p27, and mdm2 proteins and mRNAs were<br/> higher in toxicant-treated groups than those of the control. Immunohistochemical analysis revealed staining intensities of the PCNA, cyclin D1, c-myc and mdm2 protein- treated lungs and livers were stronger than those of the control group. Our results showed that combined treatment of ozone with NNK/DBP altered the cell cycle control through instability of the wild-type p53 gene. Such pivotal p53-mediated cell cycle alterations may be responsible for the toxicity observed under our experimental condition. These results may be applied to risk assessment of mixture-induced toxicity.