Target intelligence / Profile preview

Reactive oxygen and nitrogen species–generating pathways (RONS-generating pathways)

Target
RONS-generating pathways
Molecular classification
Enzyme, Metabolic pathway
01

Overview

Reactive oxygen and nitrogen species (RONS)–generating pathways represent a complex network of biochemical processes that produce highly reactive molecules, including superoxide, hydrogen peroxide, and nitric oxide (Di Meo et al., 2016). These species are primarily generated by specialized enzymes such as NADPH oxidases (NOX), nitric oxide synthases (NOS), and xanthine oxidase, as well as as byproducts of mitochondrial respiration (Bedard & Krause, 2007). Under physiological conditions, RONS serve as critical secondary messengers in signal transduction and are essential for the immune system's ability to kill pathogens via the respiratory burst. However, excessive production or inadequate neutralization leads to oxidative and nitrosative stress, which causes cumulative damage to cellular macromolecules like DNA, proteins, and lipids. This damage is a hallmark of various chronic diseases, including atherosclerosis, Alzheimer's disease, and various cancers (Förstermann & Sessa, 2012). Pharmacological intervention focuses on inhibiting specific RONS-producing enzymes or utilizing scavengers to neutralize excess species, though maintaining the delicate balance of redox homeostasis remains a significant therapeutic challenge (Sies et al., 2017).

Other names
ROS/RNS production pathwaysOxidative stress pathwaysPro-oxidant pathwaysRedox-generating systemsReactive oxygen species metabolic process
02

Mechanism of action

Inhibition of specific RONS-generating enzymes such as NADPH oxidase (NOX), xanthine oxidase (XO), or nitric oxide synthase (NOS) to reduce the production of reactive species and mitigate oxidative/nitrosative stress, or the use of scavengers to neutralize existing reactive molecules.

03

Biological functions

Signal transductionImmune responseApoptosisRedox signalingCellular homeostasisVasodilation regulation
04

Disease associations

CancerInflammationNeurodegenerative diseaseCardiovascular diseaseDiabetesInfectionAtherosclerosis
05

Safety considerations

Impairment of physiological redox signalingSuppression of innate immune response (e.g., phagocytic oxidative burst)Potential for off-target effects due to broad enzyme inhibitionRisk of disrupting essential nitric oxide-mediated vasodilation and blood pressure regulationAntioxidant paradox where excessive suppression of RONS increases mortality
06

Interacting drugs

Allopurinol

7 more in the full profile.

07

Biomarkers

Malondialdehyde (MDA)8-isoprostane8-hydroxy-2'-deoxyguanosine (8-OHdG)3-nitrotyrosineGlutathione (GSH/GSSG) ratioProtein carbonyls

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