ToxSci Advance Access published online on May 24, 2004
Toxicological Sciences, doi:10.1093/toxsci/kfh173
Toxicological Sciences © Society of Toxicology 2004; all rights reserved
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1 School of Pharmacy, Taipei Medical University, Taipei, Taiwan
* To whom correspondence should be addressed. E-mail: jjkang{at}ha.mc.ntu.edu.tw.
The genotoxic potency of motorcycle exhaust particles (MEP) was investigated by use of a bacterial reversion assay, and chromosome aberration and micronucleus test in this study. In the bacterial reversion assay (Ames test), MEP concentration-dependently increased TA98, TA100, and TA102 revertants in the presence of metabolic activating enzymes. In the chromosome aberration test, MEP concentration-dependently increased abnormal structural chromosomes in CHO-K1 cells both with and without S-9. Pretreatment with antioxidants (
Accepted May 7, 2004
Genetic Toxicology
Genotoxicity of Motorcycle-Exhaust Particulate in Vivo and in Vitro
2 Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan
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Abstract
-tocopherol, ascorbate, catalase, and NAC) showed varying degrees of inhibitory effect on the MEP-induced mutagenic effect and chromosome structural abnormalities. In the in vivo micronucleus test, MEP dose-dependently induced micronucleus formation in peripheral red blood cells after 24 and 48 h of treatment. The increase of micronucleated reticulocytes induced by MEP can be inhibited by pretreatment with
-tocopherol and ascorbate. The fluorescence intensity of DCFH-DA loaded CHO-K1 cells were increased upon addition of MEP. Our data suggest that MEP can induce genotoxicity through a reactive oxygen species (ROS)-dependent pathway, which can be augmented by metabolic activation.
-Tocopherol, ascorbate, catalase, and NAC can inhibit MEP-induced genotoxicity, indicating that reactive oxygen species might be involved in this effect.![]()
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