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Reactive oxygen species (ROS) balance, also known as redox homeostasis, refers to the delicate equilibrium between the production of highly reactive oxygen-containing molecules and the biological system's ability to detoxify these intermediates or repair the resulting damage (Sies, H., 2017, Redox Biology). ROS, such as superoxide anions and hydrogen peroxide, are natural byproducts of mitochondrial respiration and enzymatic activities like those of NADPH oxidases. While low levels of ROS are essential for cellular signaling, proliferation, and immune defense, an imbalance—termed oxidative stress—leads to the damage of proteins, lipids, and DNA (Pizzino, G., et al., 2017, Oxidative Medicine and Cellular Longevity). This state is a hallmark of numerous pathologies, including cancer, neurodegeneration, and cardiovascular disease. Therapeutic strategies aimed at restoring ROS balance typically involve the administration of exogenous antioxidants or the activation of endogenous pathways like Nrf2 to enhance cellular defenses (Forman, H. J., & Zhang, H., 2021, Nature Reviews Drug Discovery). However, this is not a single molecular target but a complex physiological process, making precise pharmacological intervention challenging due to the risk of inducing reductive stress or disrupting vital signaling pathways.
Modulation of ROS balance is achieved through the direct scavenging of free radicals, the pharmacological induction of endogenous antioxidant enzymes via the Nrf2-KEAP1 pathway, or the targeted inhibition of ROS-generating enzymes such as NADPH oxidases (NOX) and xanthine oxidase (Sies, H., & Jones, D. P., 2020, Nature Reviews Molecular Cell Biology).
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