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Reactive oxygen species (ROS) and redox buffers constitute a fundamental biochemical system responsible for maintaining cellular redox homeostasis. ROS, such as superoxide anions and hydrogen peroxide, are natural byproducts of aerobic metabolism and function as secondary messengers in various signaling pathways, including MAPK and NF-κB [PMID: 28129551]. To prevent oxidative damage to lipids, proteins, and DNA, cells utilize redox buffers like glutathione (GSH) and thioredoxin (Trx), along with specialized enzymes such as superoxide dismutase (SOD) and catalase [PMID: 30585954]. An imbalance between ROS production and antioxidant defense leads to oxidative stress, which is a hallmark of numerous pathologies, including cancer, neurodegenerative disorders, and cardiovascular diseases [PMID: 24591657]. Pharmacological intervention typically aims to either bolster antioxidant defenses using precursors like N-acetylcysteine or, conversely, to deplete redox buffers in cancer cells to trigger oxidative-stress-induced apoptosis [PMID: 31132351].
Direct scavenging of reactive species, replenishment of endogenous antioxidant pools, and transcriptional upregulation of antioxidant response elements via the Nrf2 pathway.
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