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Oxidative stress markers and redox systems encompass the collective network of enzymes, antioxidants, and signaling pathways that maintain cellular redox balance. This system includes key enzymatic components such as superoxide dismutase (SOD), catalase, and the glutathione and thioredoxin systems, which function to neutralize reactive oxygen species (ROS) generated during metabolic processes (MDPI, 2024). When the production of ROS overwhelms these antioxidant defenses, oxidative stress occurs, leading to the damage of cellular macromolecules like lipids, proteins, and DNA. This damage is quantified through specific biomarkers, including malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG), and protein carbonyls, which serve as indicators of oxidative stress levels in clinical and research settings (NIH, 2024). Dysregulation of redox homeostasis is a critical driver in the progression of various diseases, including cancer, neurodegeneration, and cardiovascular disorders. Therapeutic strategies targeting these systems involve either the activation of antioxidant pathways, such as the Nrf2-Keap1 axis (e.g., bardoxolone methyl), or the targeted inhibition of redox enzymes to selectively kill cancer cells (e.g., auranofin targeting thioredoxin reductase) (Frontiers, 2023). However, the therapeutic window is often narrow because ROS also serve as essential signaling molecules for normal physiological functions like immune response and cell proliferation (PubMed, 2022).
Modulation of reactive oxygen species (ROS) levels through direct scavenging, activation of antioxidant transcription factors (e.g., Nrf2), or inhibition of specific redox-regulating enzymes (e.g., Thioredoxin reductase).
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