Quinoid polycyclic aromatic hydrocarbons-mediated production of reactive oxygen species and subsequet activation of NF-κB and induction of cyclooxygenase-2
Tobacco smoke and the atmosphere consist of a wide variety of compounds with adverse health effects. Polycyclic aromatic hydrocarbons (PAHs) are principal toxic compounds. Some of PAHs containing oxygen (quinoid PAHs) generate reactive oxygen species (ROS) through enzymatic and nonenzymatic redox cycling reactions. ROS can cause severe oxidative stress leading to various diseases such as cancer and inflammation. In this study, we estimated the intracellular ROS production and nuclear factor kappa B (NF-κB) translocation in A549 cells exposed to isomers of quinoid PAHs having two to four rings. We found that both acenaphthenequinone (AcQ) and phenanthrene-9,10-quinone (PQ) enhanced ROS generation and that AcQ translocated NF-κB from the cytosol to the nucleus. In addition, AcQ induced cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) production were mediated by the activation of NF-κB. Upregulation of NF-κB and COX-2 expression and PGE2 production by AcQ treatment was suppressed by the antioxidant N-acetylcysteine. These results provide that AcQ might play an important role in human lung cancer and inflammatory diseases.研究ノート (Note
