Apigenin Induces Alterations of Reactive Oxygen Species, Ca(superscript +2) and Mitochondria Membrane Potential in Human Lung Cancer H460 and A549 Cells

Abstract

Lung cancer is a leading cause of cancer death in the United States and Taiwan. Currently, the mortality rates in lung cancer patients remain high. Numerous evidences have demonstrated that natural compounds contain chemopreventive and chemotherapeutic functions. Apigenin (4, 5, 7-trihydroxyflavone), a promising chemopreventive agent presented in fruits and vegetables, has been shown to induce cell cycle arrest and apoptosis in many types of human cancer cell lines. In the present studies, H460 and A549 cells were treated with apigenin and then were analyzed for alterations of reactive oxygen species (ROS), Ca(superscript +2) and mitochondria membrane potential (MMP). The results indicated that H460 cells treated with 120 μM apigenin for 10 min to 3 hr led to the ROS production up to 3 h treatment. We also found that ROS for A549 cells was higher in the apigenin treated groups. The ROS production was maximal at 24hr after treatment. H460 cells treated with 120 μM apigenin for 0-4 h will lead to cytoplasmic Ca(superscript +2) increased for up to 2 h treatment. Increasing the time of apigenin treatment from 24 to 72 hr led to slightly increase in the Ca+(superscript +2)2 production in A-549 cells. The MMP was led to slightly reduction in the apigenin-treated groups for 6hr than in the control in H460 cells. Increasing the reaction periods of time of apigenin led to greater reduction of the MMP in A-549 cells during 1 hr. We may conclude that apigenin treatment decreased the levels of MMP and increased the productions of ROS and Ca(superscript +2) in H460 and A549 cells.