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Oxidative stress components refer to a heterogeneous group of molecules involved in the generation and neutralization of reactive oxygen and nitrogen species (ROS/RNS) [1]. This collective includes pro-oxidant enzymes like NADPH oxidase, antioxidant enzymes such as superoxide dismutase (SOD) and catalase, and low-molecular-weight antioxidants like glutathione [2]. These components are essential for maintaining redox homeostasis, which regulates critical cellular processes including signal transduction, gene expression, and apoptosis [3]. When the production of reactive species exceeds the capacity of the antioxidant defense system, oxidative stress occurs, leading to oxidative damage of lipids, proteins, and nucleic acids [4]. This pathological state is implicated in the progression of various conditions, including neurodegenerative diseases, cardiovascular disorders, and chronic inflammation [5]. Pharmacological intervention typically aims to restore redox balance through the administration of exogenous antioxidants or the activation of endogenous pathways like the Nrf2-ARE signaling axis [6]. However, therapeutic success is often limited by the complexity of redox signaling and the risk of inducing reductive stress [7]. Sources: [1] Sies H, et al. (2020) Nat Rev Mol Cell Biol; [2] Halliwell B, Gutteridge JMC. (2015) Free Radicals in Biology and Medicine; [3] Pizzino G, et al. (2017) Oxid Med Cell Longev; [4] Forman HJ, Zhang H. (2021) J Biol Chem; [5] He F, et al. (2020) Front Pharmacol; [6] Yamamoto M, et al. (2018) Physiol Rev; [7] Ursini F, et al. (2016) Free Radic Biol Med.
Direct scavenging of reactive oxygen species, induction of endogenous antioxidant enzymes via Nrf2 pathway activation, and inhibition of ROS-generating enzymes.
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