Perturbation of glutathione (GSH) homeostasis precipitates apoptosis by severely compromising mitochondrial integrity, leading to the depolarization of the mitochondrial membrane and the subsequent translocation of pro-apoptotic signaling molecules. This recalibration of the cellular redox environment drives cancer cells beyond their oxidative tolerance threshold, overwhelming their capacity to neutralize reactive oxygen species (ROS). Consequently, this strategy exploits the inherent redox instability of malignant cells to trigger the caspase cascade and initiate programmed cell death via the intrinsic pathway.