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Cellular macromolecules leading to ROS generation refers to a broad category of biological entities, including proteins, lipids, and nucleic acids, that contribute to the production of reactive oxygen species (ROS) under various physiological and pathological conditions [1][3]. ROS generation typically occurs via the leakage of electrons from the mitochondrial respiratory chain or through the catalytic activity of enzymes such as NADPH oxidases (NOX) and xanthine oxidase [2]. In pharmacology, this process is often exploited by pro-oxidant drugs, such as anthracyclines and arsenic trioxide, which induce high levels of ROS to trigger apoptosis in cancer cells [4][6]. However, excessive ROS production can also lead to non-specific damage to DNA, proteins, and membranes, contributing to the pathogenesis of neurodegenerative and cardiovascular diseases [3][5]. Because this term describes a collective mechanism or a state of oxidative stress involving multiple distinct molecular components rather than a single specific protein or receptor, it is classified as a descriptive functional category rather than a discrete therapeutic target [5].
Induction of oxidative stress through redox cycling, mitochondrial electron leakage, or enzymatic activation (e.g., NADPH oxidase) resulting in macromolecular damage and programmed cell death.
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