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Oxidative-nitrosative stress is a pathological state resulting from excess reactive oxygen species (ROS) and reactive nitrogen species (RNS) overwhelming cellular antioxidant systems, leading to protein, lipid, and DNA damage, cell death, and the progression of various diseases[1][2][3][4][5]. It is not a molecule or receptor but rather a dynamic cellular condition featuring numerous interrelated molecular events and modifications, such as tyrosine nitration, lipid peroxidation, and depletion of endogenous antioxidants. Therapeutic intervention typically aims to rebalance redox homeostasis or mitigate downstream oxidative and nitrosative damage rather than interacting with a single gene, receptor, or enzyme.
Drugs act through: - Scavenging ROS/RNS - Inhibiting ROS/RNS generation - Enhancing endogenous antioxidant defenses - Reducing protein/lipid/DNA oxidation and nitration
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