https://scholars.lib.ntu.edu.tw/handle/123456789/343157
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kuo, Min-Liang | en_US |
dc.contributor.author | SHIOU-HWA JEE | en_US |
dc.contributor.author | Chou, Ming-Hong | en_US |
dc.contributor.author | Ueng, Tzuu-Huei | en_US |
dc.creator | Kuo, M.-L. and Jee, S.-H. and Chou, M.-H. and Ueng, T.-H. | - |
dc.date.accessioned | 2018-09-10T07:10:01Z | - |
dc.date.available | 2018-09-10T07:10:01Z | - |
dc.date.issued | 1998-03 | - |
dc.identifier.uri | http://www.scopus.com/inward/record.url?eid=2-s2.0-0032536707&partnerID=MN8TOARS | - |
dc.identifier.uri | http://scholars.lib.ntu.edu.tw/handle/123456789/343157 | - |
dc.description.abstract | In this study, we investigated the involvement of reactive oxygen species (ROS) in the motorcycle exhaust particle (MEP)-induced genotoxic and non-genotoxic activity in mammalian cell systems. Initially, the capability of MEP to induce ROS was evaluated by using 2',7'-dichlorofluorescin diacetate (DCFH-DA) to detect hydrogen peroxide (H2O2). A five-fold increase in H2O2 was observed in Chinese hamster lung V79 and human lung carcinoma Calu-1 cells treated with 100 μg/ml MEP for 2 h. Under the same experimental conditions, only a two-fold elevation in H2O2 was detected in hepatic cell systems such as BNL.Cl.2, HepG2, and Hep3B. Treatment of the V79 cells with varying concentrations of MEP caused a dose-dependent increase in sister chromatid exchanges (SCEs), which are effectively inhibited by addition of antioxidants, N-acetyl-L-cysteine (NAC) and ascorbic acid. Furthermore, we determined the oxidized bases in the V79 cells after exposure to MEP. The result showed that 500 μg/ml MEP induced a 3.7-fold increase in thymine glycol (TG) and a seven-fold increase in 8-hydroxy-guanosine (8-OHGua) as compared to untreated cells. We subsequently examined whether MEP would affect gap junctional intercellular communication (GJIC), a tumor promotion process, in V79 cells. We found that MEP inhibited GJIC in a dose-response fashion. Maximal inhibition occurred at 500 μg/ml. The concentration that inhibited at 0.5 of the fraction of the control was 200 μg/ml. Interestingly, when cells were pretreated with NAC or ascorbic acid, they could abolish the MEP-mediated inhibition of GJIC. In addition, a moderate decrease of glutathione was observed in the V79 cells during exposure to MEP. Taken together, our findings suggest that MEP can induce oxidative stress in a broad range of cell lines, especially in lung cell systems. The MEP-induced oxidative stress was critically involved in both genotoxic and non-genotoxic activity. | en_US |
dc.language | en | en |
dc.language.iso | en | en_US |
dc.relation.ispartof | Mutation Research - Genetic Toxicology and Environmental Mutagenesis | en_US |
dc.source | AH-Scopus to ORCID | - |
dc.subject | Gap junctional intercellular communication (GJIC); Glutathione; Motorcycle emission particles (MEP); Oxidative stress; Sister chromatid exchange (SCE) | en_US |
dc.title | Involvement of oxidative stress in motorcycle exhaust particle-induced DNA damage and inhibition of intercellular communication | en_US |
dc.type | journal article | en_US |
dc.identifier.doi | 10.1016/S1383-5718(98)00020-5 | - |
dc.relation.pages | 143-150 | en_US |
dc.relation.journalvolume | 413 | en_US |
dc.relation.journalissue | 2 | en_US |
item.fulltext | no fulltext | - |
item.openairetype | journal article | - |
item.languageiso639-1 | en | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | Dermatology | - |
crisitem.author.orcid | 0000-0001-6737-6297 | - |
crisitem.author.parentorg | College of Medicine | - |
Appears in Collections: | 醫學系 |
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