Abstract
Ozone (O3) is a natural, highly unstable atmospheric gas that rapidly decomposes to oxygen. Although not being a radical molecule, O3 is a very strong oxidant and therefore it is potentially toxic for living organisms. However, scientific evidence proved that the effects of O3 exposure are dose-dependent: high dosages stimulate severe oxidative stress resulting in inflammatory response and tissue injury, whereas low O3 concentrations induce a moderate oxidative eustress activating antioxidant pathways. These properties make O3 a powerful medical tool, which can be used as either a disinfectant or an adjuvant agent in the therapy of numerous diseases. In this paper, the cellular mechanisms involved in the antioxidant response to O3 exposure will be reviewed with special reference to the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) and its role in the efficacy of ozone therapy.
Highlights
Ozone (O3) is a natural gas forming from dioxygen (O2) by the action of ultraviolet lighetleacntdrical discharges in electrical discharges in the atmosphere; O3 is highly instable, rapidly breaking downdtioatiotsmic allotrope
It occurs in very low amounts in the atmosphere comparedOto3 iOs 2k.nown as a strong O3 is known as a strong oxidant being at the same time a dangerous respiratory hazard and polcluotnatnritbuting to several contributing to several diseases; it is a powerful oxidizing agentmwanitihfold industrial app manifold industrial applications9[]6a–n9d] consumer implem and consumer implementations [10,11,12,13]
Oxidative stress is due to the accumulation of reactive oxygen species (ROS) (O2−, H2O2 and OH), that are generated as by-products of either physiological or exogenous stress factors
Summary
Ozone (O3) is a natural gas forming from dioxygen (O2) by the action of ultraviolet lighetleacntdrical discharges in electrical discharges in the atmosphere; O3 is highly instable, rapidly breaking downdtioatiotsmic allotrope. Exposure to toxic levels of atmospheric O3 induces injury and inflammation through activation of the redox sensitive nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), which is one of the main players in transcribing pro-inflammatory cytokines and, in turn, in increasing the expression of several proteins involved in the antioxidant response [47,57,58,59,60,61,62,63,64,65]. O2-O3 therapy proved to be beneficial for the treatment of diabetic complications and spinal pain by activating various antioxidant pathways involving hypoxia inducible factor-1α (HIF-1α), nuclear factor of activated T-cells (NFAT), activated protein-1 (AP-1) pathways, and Nrf2 [75] Based on these observations, it was hypothesized that the antioxidant and anti-inflammatory effects of low O3 concentrations involve activation of Nrf, which is considered as a key factor for the efficacy of O2-O3 treatments [76,77,78]. M1. aiMn afuinnctfiuonncatlipoantahlwpaaytshdwepayens ddinegpoenndNinrfg aocntivaNtirofn inadctuivceadtiobny loinwdouzcoende cboyncelonwtratoioznosn.e Acroronwcesnitnrdatiicoantes.uApr-r(orweds)ionrddicoawtenu-p(b- l(ureed) )reogrudlaotwionn-. (blue) regulation
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