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"Pro-apoptotic pathways via reactive oxygen species generation" refer to a set of cellular signaling mechanisms wherein elevated levels of reactive oxygen species (ROS) induce apoptosis, primarily through mitochondrial and death receptor-mediated processes. ROS can damage cellular components, disrupt mitochondrial membrane potential, promote cytochrome c release, and activate both intrinsic (mitochondrial) and extrinsic (death receptor) apoptotic pathways. These pathways are of biomedical interest since many cancer and neurodegenerative diseases involve altered ROS/apoptosis signaling, but 'pro-apoptotic pathways via ROS generation' is not a single defined molecule or canonical drug target—it encompasses a broad mechanism relevant to multiple molecular players and diseases
Drug-induced elevation of ROS to pro-apoptotic levels (pro-oxidants), caspase activation, intrinsic and extrinsic apoptotic pathway activation, mitochondrial membrane permeabilization, and sometimes inhibition of antioxidant defense
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