Reactive oxygen species-related pathways and antioxidant mechanisms (ROS/Antioxidant pathways)

Reactive oxygen species (ROS)-related pathways and antioxidant mechanisms constitute a complex network responsible for maintaining cellular redox homeostasis (Sies et al., 2017). ROS, including superoxide anions and hydrogen peroxide, are produced as natural byproducts of mitochondrial metabolism and by specific enzymes like NADPH oxidases (Holmström & Finkel, 2014). While low levels of ROS act as essential signaling molecules for cell proliferation and differentiation, excessive accumulation leads to oxidative stress, causing damage to DNA, proteins, and lipids (Forman & Zhang, 2021). The antioxidant defense system, primarily regulated by the Nrf2-KEAP1 pathway, employs enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase to neutralize these reactive species (Hayes & Dinkova-Kostova, 2014). Dysregulation of these pathways is a hallmark of numerous pathologies, including cancer, neurodegeneration, and cardiovascular diseases. Therapeutic strategies often focus on enhancing antioxidant capacity through Nrf2 activators or direct ROS scavengers, though clinical success has been limited by the antioxidant paradox, where excessive suppression of ROS can disrupt vital physiological processes (Sies et al., 2017).

Other names

Redox signaling pathwaysAntioxidant defense systemOxidative stress responseROS scavenging system

Modulation of redox-sensitive transcription factors, such as the activation of Nuclear factor erythroid 2-related factor 2 (Nrf2) to induce antioxidant response element (ARE)-driven genes, direct scavenging of free radicals by small molecules, and targeted inhibition of ROS-generating enzymes like NADPH oxidase (NOX) (Hayes & Dinkova-Kostova, 2014; Sies et al., 2017).