Figure 14

Proposed mechanism of action for the antitumor activity of hmxbato against A549 lung tumor cells. The interaction of hmxbato with cell DNA causes an oxidative stress which results in increased ROS production. The ROS overproduction induces the activation of the intrinsic apoptotic pathway due to changes in the mitochondrial potential. The mitochondrial damage results in cytochrome C release in the cytosol with subsequent caspase-9 activation. The caspase-9 promotes the caspase-3 activation, which will activate the enzyme PARP-1. Finally, the cell death is induced by apoptosis, justifying the following cellular events: (1) changes in mitochondrial potential; (2) cell cycle arrest; (3) morphological changes; (4) inhibition of cell proliferation and (5) DNA damage.