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Cellular targets mediating oxidative injury represent a diverse group of molecular entities and pathways involved in the generation and regulation of reactive oxygen species (ROS). This category includes ROS-producing enzymes such as the NADPH oxidase (NOX) family and xanthine oxidase, as well as the mitochondrial electron transport chain, which serves as a major source of endogenous superoxide (Bedard & Krause, 2007). Conversely, it encompasses the cellular antioxidant defense systems, including enzymes like superoxide dismutase (SOD), catalase, and glutathione peroxidase, along with the Nrf2-KEAP1 signaling axis that regulates the expression of protective genes (Kansanen et al., 2013). Oxidative injury occurs when an imbalance between ROS production and antioxidant capacity leads to the oxidative modification of lipids, proteins, and nucleic acids, a process central to the pathogenesis of neurodegenerative diseases, cardiovascular disorders, and cancer (Sies et al., 2017). Therapeutic approaches targeting these mediators often involve the use of ROS scavengers, inhibitors of ROS-generating enzymes, or pharmacological activators of endogenous antioxidant pathways to restore redox homeostasis. However, a significant challenge in targeting these systems is the need to mitigate pathological oxidative stress without disrupting essential physiological redox signaling required for normal cellular function.
Activation of Nrf2-mediated antioxidant response; inhibition of ROS-generating enzymes such as NADPH oxidase; direct scavenging of reactive oxygen and nitrogen species (Kansanen et al., 2013; Bedard & Krause, 2007).
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