Coadjustment of quercetin and hydrogen peroxide: the role of ROS in the cytotoxicity of quercetin.

Quercetin (QU) displays antioxidant and cell protective effects in most cell culture models, yet in some studies it is reported that QU shows prooxidant and cytotoxic effects. In order to explore the real role of ROS in QU's cytotoxicity, the cytotoxicity of QU and/or H2O2, as indicated by the proliferation and viability of HL-60 cells, was examined in this study. Both H2O2 and QU dose-dependently induced cell proliferation arrest and cell death. The cytotoxicity of QU could be diminished by the supplement of H2O2 in the culture medium, at the same time, the addition of QU also significantly attenuated H2O2- caused cytotoxicity. These results indicated that certain amounts of ROS are critical for the proliferation and viability of HL-60 cells, QU scavenged the necessary ROS, and hence led to the proliferation arrest and cell death; on the contrary, the excessive ROS, such as H2O2, are obviously harmful to HL-60 cells, under these conditions, QU protected cells through diminishing the excessive ROS in vivo. Thus QU exerted its effects on cells, including its cytotoxic and protective effects, mainly through its antioxidant activity. The malondialdehyde (MDA, an index of ROS level) assay further confirmed this conclusion, as the effects of QU, H2O2, or their combination on HL-60 cells were closely related with the variation of MDA amounts in vivo.