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Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are highly reactive molecules, such as superoxide, hydrogen peroxide, and nitric oxide, that are generated during mitochondrial respiration and immune activation (StatPearls, PMID: 32809354). Under physiological conditions, these species act as critical secondary messengers in signal transduction pathways that regulate cell growth, differentiation, and survival (PubMed, PMID: 24591303). However, an imbalance between the production of these species and the body's antioxidant defense mechanisms leads to oxidative stress, causing cumulative damage to DNA, proteins, and lipids (PubMed, PMID: 25653749). This oxidative damage is a central driver in the pathogenesis of chronic conditions, including atherosclerosis, Alzheimer's disease, and various cancers. Therapeutic interventions often target these pathways using antioxidants or Nrf2 activators to enhance cellular resilience, though clinical success is often hampered by the dual role of ROS in essential signaling. Because ROS/RNS are necessary for processes like vascular tone regulation and pathogen defense, non-specific suppression can lead to adverse effects or a state of reductive stress.
Neutralization of reactive species through direct scavenging or induction of endogenous antioxidant enzymes via the Nrf2/ARE signaling axis.
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