Toxicity of the spike protein of COVID-19 is a redox shift phenomenon: A novel therapeutic approach - ScienceDirect - 0 views
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COVID19 COVID-19 cancer inflammation SARS-CoV-2 spike proteins COVID spikeopathy
shared by Nathan Goodyear on 01 Sep 23
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Redox shift is due to Warburg effect and mitochondrial impairment.
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Redox shift is due to Warburg effect and mitochondrial impairment.
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Redox shift is due to Warburg effect and mitochondrial impairment.
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The cytokine storm is a consequence of mitochondrial dysfunction
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The cytokine storm is a consequence of mitochondrial dysfunction
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The cytokine storm is a consequence of mitochondrial dysfunction
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The cytokine storm is a consequence of mitochondrial dysfunction
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Lipoic acid, Methylene Blue and Chlorine dioxide relieve COVID-19 spike protein toxicity
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Lipoic acid, Methylene Blue and Chlorine dioxide relieve COVID-19 spike protein toxicity
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Lipoic acid, Methylene Blue and Chlorine dioxide relieve COVID-19 spike protein toxicity
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Lipoic acid, Methylene Blue and Chlorine dioxide relieve COVID-19 spike protein toxicity
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most diseases display a form of anabolism due to mitochondrial impairment
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most diseases display a form of anabolism due to mitochondrial impairment
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most diseases display a form of anabolism due to mitochondrial impairment
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infection by Covid-19 follows a similar pattern
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chronic inflammation
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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infection by Covid-19 follows a similar pattern
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unrelenting anabolism leads to the cytokine storm,
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unrelenting anabolism leads to the cytokine storm,
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unrelenting anabolism leads to the cytokine storm,
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chronic inflammation
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chronic inflammation
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infection by Covid-19 follows a similar pattern
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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direct consequence of redox iMeBalance, itself a consequence of decreased energy yield by the mitochondria
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direct consequence of redox iMeBalance, itself a consequence of decreased energy yield by the mitochondria
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mitochondrial dysfunction and increased levels of lactate, which are important characteristics of metabolic shift and Warburg effect in many diseases
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mitochondrial dysfunction and increased levels of lactate, which are important characteristics of metabolic shift and Warburg effect in many diseases
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increased lactate dehydrogenase activity (LDH) was observed in COVID-19 patients
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increased lactate dehydrogenase activity (LDH) was observed in COVID-19 patients
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almost every disease presents an increased anabolism
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almost every disease presents an increased anabolism
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cell division is the most sophisticated way to release entropy
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cell division is the most sophisticated way to release entropy
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transition from catabolism to anabolism is driven by a redox shift
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transition from catabolism to anabolism is driven by a redox shift
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viral spike protein binds to ACE2 receptor of the host cell [22,23].
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redox signaling plays an important role in regulating immune function and inflammation, and disruptions in this signaling can lead to excessive cytokine production and immune system activation
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Aging is associated with a poor control of the redox balance
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thiol/disulfide homeostasis
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reduced extracellular environment in the elderly and the increased susceptibility to Covid-19 infection
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reduced extracellular environment in the elderly and the increased susceptibility to Covid-19 infection
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Redox signaling tightly modulates the inflammatory response and oxidative stress has been reported in acute Covid-19
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People at high risk are the elderly, patients suffering from metabolic syndrome such as obesity, or those suffering from chronic diseases such as cancer or inflammation
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COVID-19 patients with severe disease have higher levels of oxidative stress markers and lower antioxidant levels
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oxidative stress can activate the NLRP3 inflammasome, which is a protein complex that plays a key role in the cytokine storm
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inflammation leads to the formation of ROS and RNS, while redox iMeBalance results in cellular damage, which in turn triggers an inflammatory response
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persistently elevated mtROS triggers endothelial dysfunction and inflammation, which results in a vicious loop involving ROS, inflammation, and mitochondrial dysfunction
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Damaged mitochondria releasing ROS induce inflammation via the NLRP3 inflammasome
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Damaged mitochondria releasing ROS induce inflammation via the NLRP3 inflammasome
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reduced environment during the cytokine storm
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IL-2 is highly up-regulated in Covid-19 patients [37], and IL-2 is known to significantly stimulate the generation of NO in patients
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Nitric acid is also the key mediator of IL-2-induced hypotension and vascular leak syndrome
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mitochondrial dysfunction has been linked to the pathogenesis of Covid-19
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mitochondrial dysfunction triggered by SARS-CoV-2 leads to damage to the mitochondria
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mitochondrial dysfunction triggered by SARS-CoV-2 leads to damage to the mitochondria
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As catabolism is decreased, entropy is released through anabolism
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Elevated levels of lactate, a characteristic of the Warburg effect, were also reported in the high-risk Covid-19
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elevated levels of ventricular lactic acid consistent with oxidative stress
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A decrease of ΔΨm is implicated in several inflammation-related diseases
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decrease in ΔΨm in leucocytes from Covid-19 patients
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vaccinated with RNA or DNA vaccines triggering the synthesis of the viral spike protein in human cells
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viral reactivation in varicella-zoster virus [55] or hepatitis [56], coagulopathy and resulting stroke and myocarditis following both DNA-based vaccines [57] and RNA-based vaccines
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Covid-19, mitochondrial impairment
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characteristic of the Warburg effect is present in almost every disease and appears to be a central feature in most of the hallmarks of cancer
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inflammation, mitochondrial dysfunction and increased lactate concentrations in the extracellular fluid
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In Covid-19, like any inflammation, there is a metabolic rewiring where cells rely on glycolysis
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As the mitochondria are impaired, the infected cell cannot catabolize efficiently. It will release lactic acid in the blood stream
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Striking similarities are seen between cancer, Alzheimer's disease and Covid-19, all related to the Warburg effect
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Cancer, inflammation, Alzheimer's, and Parkinson's diseases share a common peculiarity, the inability of the cell to export entropy outside the body in the harmless form of heat
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Entropy: lack of order or predictability; gradual decline into disorder.
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MEB relieves the Warburg effect [87], improves memory [77], is active in the treatment of depressive episodes [79,80] and reduces the importance of ischemic strokes
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MEB relieves the Warburg effect [87], improves memory [77], is active in the treatment of depressive episodes [79,80] and reduces the importance of ischemic strokes
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MEB has been shown to inhibit SARS-Cov-2 replication in vitro
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MEB has been shown to inhibit SARS-Cov-2 replication in vitro
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It has been shown that Covid-19-patients treated with MEB, have a significant reduction in hospital stay duration and mortality
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MeB is an acceptor-donor molecule
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MeB + can take a pair of electrons (of H atoms) and MeBH can release this pair easily, so that MeB is partially recycled like a catalyst
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MeB acts as an electron bridge between a donor (FADH2, FMNH, NADH) and an acceptor (complex IV of ETC or oxygen itself)
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As a coenzyme of pyruvate dehydrogenase (PDH), alpha-lipoic acid (ALA) initiates the formation of acetyl-CoA to feed the TCA cycle
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ALA enhances the catabolism of carbon. cycle and therefore may reduce the Warburg effect and consequently, lactate production
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Methylene Blue plays a similar role after the TCA cycle, by carrying electrons to complex IV of the electron transport chain
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Drugs such as lipoic acid and MeB, which target the metabolism, decrease the redox shift by increasing catabolism