Antioxidant enzymes and cellular oxidative stress pathways

Antioxidant enzymes and cellular oxidative stress pathways represent a collective biological system dedicated to maintaining redox homeostasis by neutralizing reactive oxygen species (ROS). This system includes primary enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, which catalyze the conversion of toxic radicals into stable molecules like water and oxygen (Ighodaro & Akinloye, 2018). The Nuclear factor erythroid 2-related factor 2 (Nrf2) serves as the master transcriptional regulator of this response, inducing the expression of numerous cytoprotective genes in response to oxidative stress (He et al., 2020). Chronic oxidative stress, characterized by an imbalance between ROS production and antioxidant capacity, is a fundamental driver of aging and diseases such as Alzheimer's, atherosclerosis, and diabetes (Sies et al., 2017). Pharmacological intervention typically involves Nrf2 activators, such as dimethyl fumarate, or synthetic mimetics of antioxidant enzymes to restore redox balance (Robledinos-Antón et al., 2019). However, the therapeutic window is narrow, as excessive suppression of ROS can interfere with essential physiological signaling or potentially support the survival of cancer cells (Forman & Zhang, 2021). Furthermore, many antioxidant therapies have struggled in clinical trials due to poor bioavailability or lack of specificity for the affected tissue (Gorrini et al., 2013). Understanding the spatial and temporal dynamics of ROS signaling remains critical for developing effective redox-based therapeutics.

Other names

Redox homeostasis pathwaysAntioxidant defense systemOxidative stress responseNrf2-Keap1 signaling pathwayROS scavenging system

Activation of the Nuclear factor erythroid 2-related factor 2 (Nrf2) mediated antioxidant response element (ARE) pathway, direct scavenging of reactive oxygen species, and replenishment of endogenous glutathione levels.