The Underrated Carbonate Radical (CO3•–) – Detoxification and Reduced Formation by Melatonin

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The Underrated Carbonate Radical (CO3•–) – Detoxification and Reduced Formation by Melatonin

Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2017, Vol 1, Issue 3

Abstract

Carbonate radicals are frequently overlooked or underrated oxidants that have a considerably larger range of action than the short-lived hydroxyl radicals. They possess sufficient reactivity for abstracting electrons or hydrogen atoms from many biomolecules. Carbonate radicals are formed in several reactions, e.g., via hydrogen abstraction from bicarbonate by a hydroxyl radical, through interaction of a formate radical with bicarbonate and, most importantly, from the peroxynitrite-carbon dioxide adduct. All these pathways of formation indicate an important role of carbon dioxide and bicarbonate levels for the generation of carbonate radicals and, therefore, many oxidizing reactions with aromates can be considerably enhanced by adding bicarbonate. Under physiological and, even more, pathophysiological conditions, high CO2/HCO3– concentrations are found in mitochondria and in situations of under-perfusion or ischemia. Increased levels of nitric oxide considerably increase via generation of peroxynitrite the formation of carbonate radicals, effects of relevance with regard to inflammation, Alzheimer’s disease, stroke, and all pathologies related to mitochondrial dysfunction. Melatonin counteracts both the formation and persistence of carbonate radicals, by down regulating inducible and neuronal NO synthases, by scavenging carbonate radicals, and by protecting mitochondria. By interaction with carbonate radicals, melatonin is converted to N1-acetyl-N2-formyl-5-methoxykynuramine (AFMK), another protective compound, which is metabolized to N1-acetyl-5-methoxykynuramine (AMK). AMK also down regulates inducible and neuronal NO synthases and scavenges carbonate radicals as well as various reactive oxygen species.Damage to biomolecules by reactive oxygen species is often attributed to the hydroxyl radical, because of its particularly high reactivity that enables this intermediate to interact with countless other compounds. However, the high reactivity leads to the consequence of a very short half-life of about a nanosecond and, thus, of an extremely short range of action. The carbonate radical (CO3•–) differs considerably in this regard. Despite its lower reactivity, it is still capable of abstracting electrons or hydrogen atoms from the same molecules that would undergo these reactions with hydroxyl radicals. While the awareness of damage by hydroxyl radicals is widely present in the community, this is not the case with regard to carbonate radicals. However, it seems important to direct researchers’ attention to the pathophysiological relevance of CO3•–, especially because of the fact that this symmetric radical, by virtue of resonance stabilization, has a much longer lifetime and, thus, a more far-reaching action [1].

Authors and Affiliations

Hardeland Rüdiger

Keywords

Carbonate Radical; Ischemia; Mitochondria; Peroxynitrite; Tyrosine nitration

EP ID EP570522
DOI 10.26717/BJSTR.2017.01.000264
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