Abstract
It is well known that aging and its associated diseases, including cancer, are triggered by oxidative damage to biological macromolecules. However, antioxidant compounds are still disappointingly distant from any clinical application, so that Jim Watson has declared that antioxidant supplementation may have caused more cancers than it has prevented Watson J ((2013) Oxidants, antioxidants and the current incurability of metastatic cancers Open Biol 3 DOI: 10.1098/rsob.120144).To clarify this paradox, here, we describe the mechanisms of oxidative stress focusing in particular on redox balance and physiological oxidative signals.
Highlights
Here, we describe the mechanisms of oxidative stress focusing in particular on redox balance and physiological oxidative signals
Since the last three decades, the establishment of pre-clinical evidence showing that antioxidants protect deoxyribo nucleic acid (DNA) from being damaged by oxygen free radicals, potentially preventing the genetic mutations that cause cancer [9]
reactive oxygen species (ROS) are usually considered as a side effect of aerobic metabolism, and mitochondrial respiration is thought to be the main intracellular source of accidental ROS [30]
Summary
Oxidative stress indicates a condition occurring when oxidising substances accumulate and accidental oxidative reactions thrive. In mammals, such as in all aerobic eukaryotes, the molecules with substantial oxidising potential contain oxygen. Both reactive oxygen species (ROS), including singlet O2, superoxide anion (O2−), hydrogen peroxide (H2O2), and hydroxyl radical (OH−), and reactive nitrogen species (RNS), including peroxynitrite (ONOO−), nitrogen dioxide (NO2), and dinitrogen trioxide (N2O3), are potent oxidising agents in living organisms [2]. The accumulation of ROS and, subsequently, RNS increases the chance of formation of oxidative modifications in proteins, resulting in protein carbonyl content and oxidised- or nitro-modified residues, in lipids, generating hydroperoxide lipid derivatives, and in both purines and pyrimidines, inducing DNA adducts and breaks. The rise of oxidative attacks to biological macromolecules leads to the dysfunctions of proteins, membranes, and nucleic acids
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