ToxSci Advance Access originally published online on November 2, 2006
Toxicological Sciences 2007 95(2):348-355; doi:10.1093/toxsci/kfl150
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An Environmental Quinoid Polycyclic Aromatic Hydrocarbon, Acenaphthenequinone, Modulates Cyclooxygenase-2 Expression through Reactive Oxygen Species Generation and Nuclear Factor Kappa B Activation in A549 Cells
* Graduate School of Natural Science and Technology, Kanazawa University, Kanazawa 920-1192, Japan
College of Pharmacy, Pusan National University, Busan 609-735, Korea
Faculty of Pharmaceutical Sciences, Doshisha Women's College, Kyoto 610-0395, Japan
1 To whom correspondence should be addressed at Graduate School of Natural Sciences and Technology, Kanazawa University, Kakuma-machi, Kanazawa 920-1192, Japan. Fax: +81-76-234-4456. E-mail: chungsw{at}p.kanazawa-u.ac.jp.
Received July 26, 2006; accepted October 24, 2006
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Abstract |
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Diesel exhaust particles (DEPs) contain oxygen-containing polycyclic aromatic hydrocarbons (PAHs) called quinoid PAHs. Some quinoid PAHs generate free radicals as they undergo enzymatic and nonenzymatic redox cycling with their corresponding semiquinone radicals. Reactive oxygen species (ROS) produced by these reactions can cause severe oxidative stress connected with inflammatory processing. Although humans and animals are continuously exposed to these chemicals in the environment, little is known about which quinoid PAHs are active. In this study, we estimated the intracellular ROS production and nuclear factor kappa B (NF-
B) translocation in A549 cells exposed to isomers of quinoid PAHs having two to four rings. We found that both acenaphthenequinone (AcQ) and 9,10-phenanthrenequinone (PQ) enhanced ROS generation and that AcQ translocated NF-B from the cytosol to the nucleus. However, PQ, which has been reported to induce apoptosis, did not influence NF-B activation. In addition, AcQ induced cyclooxygenase-2 (COX-2) expression which is a key enzyme in the inflammatory processing involved in the activation of NF-B. Upregulation of NF-B and COX-2 expression by AcQ treatment was suppressed by the antioxidant N-acetylcysteine (NAC). These results provide that AcQ might play an important role in human lung inflammatory diseases as an air pollutant.
Key Words: quinoid PAHs; ROS; NF-B; COX-2.
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