Oxidative stress regulators and antioxidant enzymes

Oxidative stress regulators and antioxidant enzymes constitute a complex network of proteins responsible for maintaining cellular redox homeostasis by neutralizing reactive oxygen species (ROS) and reactive nitrogen species (RNS) [1]. This category includes primary enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx), which catalyze the breakdown of free radicals, as well as master regulatory proteins like Nuclear factor erythroid 2-related factor 2 (Nrf2) that coordinate the transcriptional response to oxidative stress [2]. Under physiological conditions, these systems protect cellular components—including DNA, lipids, and proteins—from oxidative damage; however, their insufficiency or dysregulation is a central feature of chronic diseases such as Alzheimer's disease, atherosclerosis, and various cancers [3]. Pharmacological strategies often target this system by using Nrf2 activators like dimethyl fumarate to bolster endogenous defenses or by employing antioxidant mimetics to reduce oxidative burden [4]. Despite their therapeutic potential, drug development is complicated by the dual role of ROS as essential signaling molecules, where excessive inhibition can lead to 'reductive stress' and impaired cellular function [5]. [1] Sies, H. (2017). Redox Biology. [2] He, F., et al. (2020). Frontiers in Physiology. [3] Halliwell, B., & Gutteridge, J. M. C. (2015). Free Radicals in Biology and Medicine. [4] Gold, R., et al. (2012). New England Journal of Medicine. [5] Forman, H. J., & Zhang, H. (2021). Nature Reviews Drug Discovery.

Other names

Antioxidant defense systemRedox regulatorsROS scavenging enzymesEndogenous antioxidant system

Activation of the Nrf2-Keap1 signaling pathway to induce antioxidant response element (ARE)-driven genes; direct scavenging of reactive oxygen species; enzymatic conversion of superoxide radicals to hydrogen peroxide and subsequently to water; replenishment of endogenous glutathione pools.