Ozone Autohemotherapy: Possible Mechanisms of Anti-Viral Action and Anti Oxidative

Por Administrator
en Blog
en 02 Junio 2020

Ozone Autohemotherapy: Possible Mechanisms of Anti-Viral Action and Anti Oxidative

 

Introduction

While ozone is the trigger, several blood compo-nents such as erythrocytes, lymphocytes, monocytes, polymorphonuclear leukocytes, platelets, and plasma components act as substrates and are responsible for setting in motion a number of biological effects that, directly or indirectly, are responsible for the clinical im-provement observed after the autohaemotherapeutic treatment in chronic viral diseases [1].
Upon beginning O3 therapy, a multifaceted endoge-nous cascade is initiated and releases biologically active substrates in response to the transient, and moderate, oxidative stress that O3 induces. O3 can cause this mild oxidative stress because of its ability to dissolve in the aqueous component of plasma [2]. By reacting with polyunsaturated fatty acids (PUFA) and water, O3 cre-ates hydrogen peroxide (H2O2), a reactive oxygen spe-cies (ROS). Simultaneously, O3 forms a mixture of lipid ozonation products (LOP) [3]. The LOPs created after O3 exposure include lipoperoxyl radicals, hydroperoxides, malondialdehyde, isoprostanes, the ozonide and alke-nals, and 4-hydroxynonenal (4-HNE). Moderate oxida-tive stress caused by O3 increases activation of the tran

scriptional factor mediating nuclear factor-erythroid 2-related factor 2 (Nrf2). Nrf2’s domain is responsible for activating the transcription of antioxidant response elements (ARE). Upon induction of ARE transcription, an assortment of antioxidant enzymes gains increased con-centration levels in response to the transient oxidative stress of O3. The antioxidants created include, but are not limited to, superoxide dismutase (SOD), glutathi-one peroxidase (GPx), glutathione S-transferase (GST), catalase (CAT), heme oxygenase-1 (HO-1), NADPH qui-none-oxidoreductase (NQO-1), heat shock proteins (HSP), and phase II enzymes of drug metabolism. Many of these enzymes act as free radical scavengers clinically rele-vant to a wide variety of diseases [3].
In its pharmacological effect, medical O3 follows the principle of hormesis: low concentrations (or doses) show a high efficacy, which decreases with increasing concentration [4].

 

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