transition from catabolism to anabolism is driven by a redox shift
transition from catabolism to anabolism is driven by a redox shift
viral spike protein binds to ACE2 receptor of the host cell [22,23].
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
Aging is associated with a poor control of the redox balance
thiol/disulfide homeostasis
reduced extracellular environment in the elderly and the increased susceptibility to Covid-19 infection
reduced extracellular environment in the elderly and the increased susceptibility to Covid-19 infection
Redox signaling tightly modulates the inflammatory response and oxidative stress has been reported in acute Covid-19
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
COVID-19 patients with severe disease have higher levels of oxidative stress markers and lower antioxidant levels
oxidative stress can activate the NLRP3 inflammasome, which is a protein complex that plays a key role in the cytokine storm
inflammation leads to the formation of ROS and RNS, while redox iMeBalance results in cellular damage, which in turn triggers an inflammatory response
persistently elevated mtROS triggers endothelial dysfunction and inflammation, which results in a vicious loop involving ROS, inflammation, and mitochondrial dysfunction
Damaged mitochondria releasing ROS induce inflammation via the NLRP3 inflammasome
Damaged mitochondria releasing ROS induce inflammation via the NLRP3 inflammasome
reduced environment during the cytokine storm
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
Nitric acid is also the key mediator of IL-2-induced hypotension and vascular leak syndrome
mitochondrial dysfunction has been linked to the pathogenesis of Covid-19
mitochondrial dysfunction triggered by SARS-CoV-2 leads to damage to the mitochondria
mitochondrial dysfunction triggered by SARS-CoV-2 leads to damage to the mitochondria
As catabolism is decreased, entropy is released through anabolism
Elevated levels of lactate, a characteristic of the Warburg effect, were also reported in the high-risk Covid-19
elevated levels of ventricular lactic acid consistent with oxidative stress
A decrease of ΔΨm is implicated in several inflammation-related diseases
decrease in ΔΨm in leucocytes from Covid-19 patients
vaccinated with RNA or DNA vaccines triggering the synthesis of the viral spike protein in human cells
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
Covid-19, mitochondrial impairment
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
inflammation, mitochondrial dysfunction and increased lactate concentrations in the extracellular fluid
In Covid-19, like any inflammation, there is a metabolic rewiring where cells rely on glycolysis
As the mitochondria are impaired, the infected cell cannot catabolize efficiently. It will release lactic acid in the blood stream
Striking similarities are seen between cancer, Alzheimer's disease and Covid-19, all related to the Warburg effect
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
Entropy: lack of order or predictability; gradual decline into disorder.
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
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
MEB has been shown to inhibit SARS-Cov-2 replication in vitro
MEB has been shown to inhibit SARS-Cov-2 replication in vitro
It has been shown that Covid-19-patients treated with MEB, have a significant reduction in hospital stay duration and mortality
MeB is an acceptor-donor molecule
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
MeB acts as an electron bridge between a donor (FADH2, FMNH, NADH) and an acceptor (complex IV of ETC or oxygen itself)
As a coenzyme of pyruvate dehydrogenase (PDH), alpha-lipoic acid (ALA) initiates the formation of acetyl-CoA to feed the TCA cycle
ALA enhances the catabolism of carbon. cycle and therefore may reduce the Warburg effect and consequently, lactate production
Methylene Blue plays a similar role after the TCA cycle, by carrying electrons to complex IV of the electron transport chain
Drugs such as lipoic acid and MeB, which target the metabolism, decrease the redox shift by increasing catabolism
CoQ10 can significantly extend survival, delay motor deficits and delay weight loss and attenuate the development of striatal atrophy in a transgenic mouse model of HD
Pilot study and only abstract available here: Low CoQ10 levels found in amniotic sample in preterm delivered pregnancies; not difference was found in serum levels.
low CoQ10 associated with spontaneous miscarriage in abstract. The authors of this paper found CoQ10 levels increased throughout "normal pregnancy". Only abstract available here.
CoQ10 supplementation of 150 mg in individuals with CAD found to have increased catalase activity, increased SOD activity, an increased MDA levels. This reduced oxidative stress, TC, and LDL levels.
high dose CoQ10 shown to slow disease progression in Parkinson's disease. A similar study had shown the same finding in Huntington's disease. Both are excitotoxic diseases