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Reactive oxygen species (ROS) are a collective term for highly reactive, oxygen-containing molecules such as superoxide, hydrogen peroxide, hydroxyl radical, and singlet oxygen, among others[1][2][4][5]. ROS are generated as by-products of normal cellular metabolism, particularly in mitochondria, and are also produced in response to stress, xenobiotics, cytokines, and immune activation[4][2]. Electrophilic intermediates refer to electron-deficient species (such as α,β-unsaturated aldehydes and certain lipid oxidation products) generated as secondary products from ROS reactions with biomolecules or by xenobiotic metabolism[1][3]. Both ROS and electrophilic intermediates can cause cellular damage through oxidation of DNA, proteins, and lipids, but in lower concentrations, they play crucial roles as signaling molecules for cell proliferation, survival, and stress responses[4][5]. Excessive or uncontrolled levels drive pathological processes implicated in many diseases, including cancer, neurodegeneration, cardiovascular and inflammatory diseases, and aging[1][4]. Although numerous drugs and antioxidants modulate ROS/electrophile pathways, these entities are not conventional molecular drug targets—rather, they represent a chemical class and redox process, not a defined receptor, enzyme, or transporter[1][4][5]. Note: - This entry does not refer to a single, defined molecular target (like a receptor or enzyme) but rather to a broad chemical category. Thus, it is not a "therapeutic target" in the strict sense, and this designation is incorrect for a molecular target database[1][2][4]. - If you intend to refer to a specific enzyme or protein that generates, detoxifies, or senses ROS/electrophiles (such as NADPH oxidase, superoxide dismutase, or the Nrf2 pathway), refer to that specific protein by its accepted gene or protein name.
Scavenging of reactive oxygen species; Inhibition of ROS formation; Induction of ROS to trigger cell death (pro-oxidant anticancer drugs); Modulation of redox-sensitive signaling pathways
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