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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).
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.
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