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Reactive oxygen species (ROS) generation processes encompass the biochemical pathways that produce highly reactive oxygen-containing molecules, such as superoxide radicals and hydrogen peroxide (Sies et al., 2017). These processes occur primarily within the mitochondria during oxidative phosphorylation and are also mediated by specific enzymes like NADPH oxidases (NOX) and xanthine oxidase (Lambeth, 2004). Under normal physiological conditions, ROS serve as critical signaling molecules that regulate cell growth, differentiation, and the immune system's oxidative burst (Finkel, 2011). However, the excessive production of ROS leads to oxidative stress, which causes significant damage to DNA, proteins, and lipids, contributing to the progression of cancer, neurodegeneration, and cardiovascular diseases (Halliwell & Gutteridge, 2015). Pharmacological interventions target these processes either by using antioxidants to scavenge excess ROS or by inhibiting the enzymes responsible for their production to mitigate tissue injury. Conversely, some therapeutic approaches, particularly in oncology, utilize pro-oxidant drugs to intentionally elevate ROS levels to a threshold that triggers selective apoptosis in cancer cells (Trachootham et al., 2009).
Modulation of cellular redox state through enzymatic inhibition of ROS sources (e.g., NOX or xanthine oxidase), direct scavenging of reactive intermediates by antioxidants, or the deliberate induction of lethal oxidative stress to trigger apoptosis in malignant cells.
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