Target intelligence / Profile preview

Reactive oxygen species (ROS) generation and scavenging (ROS generation and scavenging)

Target
ROS generation and scavenging
Molecular classification
Enzyme, Other
01

Overview

Reactive oxygen species (ROS) generation and scavenging refers to the complex biochemical network responsible for producing and neutralizing chemically reactive molecules containing oxygen, such as superoxide radicals and hydrogen peroxide (Sies et al., 2017, Nature Reviews Molecular Cell Biology). ROS are generated as natural byproducts of mitochondrial metabolism and by specialized enzymes like NADPH oxidases (NOX) for signaling and host defense (Forman & Zhang, 2021, Free Radical Biology and Medicine). Scavenging systems, including enzymes like superoxide dismutase (SOD), catalase, and glutathione peroxidase, maintain redox homeostasis by neutralizing excess ROS. An imbalance between generation and scavenging leads to oxidative stress, which causes damage to DNA, proteins, and lipids, contributing to the pathogenesis of cancer, neurodegeneration, and cardiovascular diseases (Pizzino et al., 2017, Oxidative Medicine and Cellular Longevity). Therapeutic interventions aim to either inhibit ROS production or enhance scavenging capacity to mitigate tissue damage. However, because ROS also serve as vital signaling molecules, non-specific targeting can lead to significant safety concerns and therapeutic challenges.

Other names
Oxidative stress regulationRedox homeostasisROS metabolismRedox signaling pathway
02

Mechanism of action

Therapeutic agents modulate this process by directly scavenging free radicals, inhibiting ROS-producing enzymes such as NADPH oxidase (NOX) and xanthine oxidase, or inducing the expression of endogenous antioxidant enzymes through the activation of the Nrf2-Keap1 signaling pathway (Pizzino et al., 2017, Oxidative Medicine and Cellular Longevity; He et al., 2017, Journal of Clinical Medicine).

03

Biological functions

Signal transductionApoptosisImmune responseCell deathOther
04

Disease associations

CancerNeurodegenerative diseaseCardiovascular diseaseInflammationOther
05

Safety considerations

Disruption of physiological redox signalingPotential for pro-oxidant effects at high dosesInterference with immune-mediated pathogen killingThe antioxidant paradox, where supplementation may increase mortality in certain populations (Bjelakovic et al., 2007, JAMA)
06

Interacting drugs

N-acetylcysteine

6 more in the full profile.

07

Biomarkers

Malondialdehyde (MDA)8-hydroxy-2'-deoxyguanosine (8-OHdG)Glutathione/Glutathione disulfide (GSH/GSSG) ratioProtein carbonyls

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