Figure 7

Schematic representation of the plausible molecular mechanism proposed for the induction of apoptosis by TTHL in MCF-7 breast cancer cells. ROS overproduction and DNA intercalaiton lead to DNA damage and mitochondrial dysfunction, resulting in the release of mitochondrial pro-death proteins. There is an incresead in the number of cells within the sub-G1 phase with a maximum at IC80. The intrinsic apoptosis pathway is initiated by lose of mitochondrial potential, which leads to release of cytochrome c. Cytochrome c binds to APAF-1 and procaspase 9, resulting in activation of initiator caspase 9 and downstream executor caspases.