Target intelligence / Profile preview

Reactive oxygen species and oxidized antioxidant pools (ROS)

Target
ROS
Molecular classification
Small molecule, Reactive intermediate, Free radical, Other
01

Overview

Reactive oxygen species (ROS) are highly reactive chemical species, including superoxide, hydrogen peroxide, and hydroxyl radicals, that are formed as natural byproducts of oxygen metabolism (Sies et al., 2017, Nature Reviews Molecular Cell Biology). Under physiological conditions, they serve as critical signaling molecules for cell growth, differentiation, and the immune response; however, an imbalance between ROS production and the body's antioxidant defenses leads to oxidative stress (Ray et al., 2012, Cell Signaling). The 'oxidized antioxidant pool' refers to the depletion of endogenous reducing agents, such as the conversion of reduced glutathione (GSH) to its oxidized form (GSSG), which occurs when ROS levels overwhelm cellular capacity (Frijhoff et al., 2015, Antioxidants & Redox Signaling). This state of oxidative stress causes cumulative damage to DNA, proteins, and lipids, contributing to the pathogenesis of cancer, neurodegeneration, and cardiovascular diseases (PubMed, PMID: 22226774). Therapeutic strategies involve using antioxidants or scavengers like N-acetylcysteine or edaravone to neutralize these species or replenish the antioxidant pools (DrugBank; FDA). Despite their therapeutic potential, targeting ROS is challenging because non-selective scavenging can disrupt vital redox-sensitive signaling pathways, often leading to limited efficacy in clinical trials (NIH, National Center for Complementary and Integrative Health).

Other names
Free radicalsOxidantsOxygen radicalsPro-oxidantsOxidative stress mediatorsReactive oxygen metabolites
02

Mechanism of action

Direct chemical scavenging of free radicals, neutralization of reactive oxygen intermediates, and restoration of the reduced state of endogenous antioxidant pools such as the glutathione and thioredoxin systems.

03

Biological functions

Cell signalingImmune responseApoptosisHomeostasisRedox regulationCell death
04

Disease associations

CancerNeurodegenerative diseaseCardiovascular diseaseInflammationAging-related pathologyIschemia-reperfusion injury
05

Safety considerations

Interference with essential physiological redox signalingPotential pro-oxidant effects at high concentrationsLack of tissue and organelle specificityPoor clinical translation due to redundant oxidative pathwaysDisruption of normal immune oxidative burst
06

Interacting drugs

N-acetylcysteine

7 more in the full profile.

07

Biomarkers

Malondialdehyde (MDA)8-hydroxy-2'-deoxyguanosine (8-OHdG)Protein carbonylsGSH/GSSG ratioF2-isoprostanesSuperoxide dismutase (SOD) activity

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