@borsabil
It doesn't matter how much air they pump in with a ventilator. It will only make things worse. The blood will not oxygenate because it can't. It's chemically impossible.
Multi-system involvement and rapid clinical deterioration are hallmarks of coronavirus disease 2019 (COVID-19) related mortality. The unique clinical phenomena in severe COVID-19 can be perplexing, and they include disproportionately severe hypoxemia ...
www.ncbi.nlm.nih.gov
In other inflammatory infections, activated neutrophils are known to release myeloperoxidase (MPO) in a natural immune response, which contributes to production of hypochlorous acid (HOCl). However, during overwhelming inflammation, HOCl competes with O2 at heme binding sites, decreasing O2 saturation. Moreover, HOCl contributes to several oxidative reactions, including hemoglobin-heme iron oxidation, heme destruction, and subsequent release of free iron, which mediates toxic tissue injury through additional generation of ROS and NO consumption.
In this translational medicine based narrative review, the following pathologic metabolic pathways, deriving from hemoglobin denaturation and iron metabolism dysregulation, are highlighted: i) decrease of functioning hemoglobin quote; ii) iron overload in cell/tissue (hyperferritinemia); iii) release of free toxic circulating heme; iv) hypoxemia and systemic hypoxia; v) reduction of nitric oxide; vi) coagulation activation; vii) ferroptosis with oxidative stress and lipoperoxidation; viii) mitochondrial degeneration and apoptosis. A few clinical syndromes may follow, such as pulmonary edema based on arterial vasoconstriction and altered alveolo-capillary barrier, sideroblastic-like anemia, endotheliitis, vasospastic acrosyndrome, and arterio- venous thromboembolism. We speculated that in COVID-19, beyond the classical pulmonary immune-inflammation view, the occurrence of an oxygen-deprived blood disease, with iron metabolism dysregulation, should be taken in consideration. A more comprehensive diagnostic/therapeutic approach to COVID-19 is proposed, including potential adjuvant interventions aimed at improving hemoglobin dysfunction, iron over-deposit and generalized hypoxic state.
In order to make oxidative stress, what do you need? Oxygen. Lots of it. Reactive oxygen species are produced by the consumption of oxygen, in fact.
Ischemia-reperfusion (IR) injury is directly related to the formation of reactive oxygen species (ROS), endothelial cell injury, increased vascular permeability, and the activation of neutrophils and platelets, cytokines, and the complement system. Several studies have confirmed the...
www.hindawi.com
Hypoxia and consequently anoxia result in a decrease in intracellular ATP and an increase in ATP degradation products, such as hypoxanthine, which generates ROS production when oxygen is reintroduced during reperfusion and/or ventilation. During ischemia, this phenomenon may occur in the lung if the alveolar oxygen tension drops below 7 mmHg [26, 27]. The absence of pulmonary blood flow leads to lipid peroxidation, even in the presence of oxygen. The mechanism of oxidative stress is different from what occurs during anoxia-reoxygenation because it is not associated with decreased ATP, and it may occur even during the period of cold ischemia in an organ stored for transplantation [28].
This is what I mean by
hitting an oxidative stress bomb with oxygen. Hitting lungs that have had prolonged hypoxia with a sudden influx of oxygen is like pulling all the control rods out of a xenon-poisoned nuclear reactor. It's a terrible idea.
I mean, it
seems like a great idea because these people have low O2 saturation and hypoxia, and because we need oxygen to make ATP (which is to say, we need oxygen to live), but the blood won't take it. Enzymes that make ROS, on the other hand, will, and that ROS will go on to aggressively oxidize lipids, leading to ferroptosis and cell death.
Lipid peroxidation is the same chemical process of electron transfer as fire, or rust. It's what bleach does when it bleaches your clothing in the washing machine; it oxidizes the shit on your clothes, breaking it down and making them appear white. It's what hydrogen peroxide does to your teeth; oxidation breaks down the material staining them, leaving them visibly white. Yes, the fats and DNA in your body can "rust" if exposed to excess ROS. That's what oxidative stress is.
Remember when Bing Liu was killed in a very suspicious murder-suicide in Pittsburgh? The guy who was,
and I quote, "on the verge of making very significant findings toward understanding the cellular mechanisms that underlie SARS-CoV-2 infection and the cellular basis of the following complications", before he died?
What was his specialty?
www.csb.pitt.edu
He single-handedly helped all of us as well as many collaborators including clinicians here and in other institutions, understand and quantitatively model many complex processes, including immune signaling events, apoptotic and ferroptotic cell death, autophagy, redox lipid programming, response to radiation and radiation therapy, systems (poly)pharmacological treatments. In recent years, he had three publications in Nature Chem Biol, three in Radiation Research, two in Scientific Reports, one in Science Signaling, one in International Journal of Molecular Sciences, and one in Frontiers in Pharmacology.
Ferroptosis and redox biology. Yep. He fucking knew too much. That's why they killed him.
@Drain Todger It’s interesting to see you post about budesonide and melatonin. I found a cool doctor that prescribed me a “COVID kit” in case I get sick. Budesonide was one of the prescriptions (I’m supposed to put it in a nebulizer). He also mentioned taking a high dose of melatonin. Additionally, he gave me scripts for albuterol, an antibiotic, ivermectin and a cough medicine. I had to get the ivermectin from a compounding pharmacy. I just wanted to let you know that some doctors agree with you on those medications.
Scientists keep making the same mistake over and over again.
"Cigarette smoke prevents COVID? It must be the nicotine! COVID-19 must be a nicotinic cholinergic disease!"
No. Cigarette smoke contains nitric oxide,
which is an antioxidant.
"Melatonin treats COVID? It must be because melatonin suppresses inflammatory cytokines!"
No. Melatonin
is an antioxidant and it also
scavenges peroxynitrite.
"Budesonide treats COVID? It must be because budesonide is an inhaled steroid and gets into the lungs quicker than injected steroids like dexamethasone!"
No. Budesonide is not just an inhaled steroid,
it's also an antioxidant.
"Famotidine treats COVID? It must be because it's a histamine blocker! Histamine activity is somehow increasing these people's inflammation!"
No. The most common H2 blockers
are all antioxidants.
"Fluvoxamine treats COVID? It must be because serotonin reuptake does something to make the virus worse!"
No. Fluvoxamine
is an antioxidant.
Almost every goddamn repurposed drug that has any benefit at all for COVID-19 is an antioxidant and can scavenge or inhibit reactive oxygen species.
That's because clinical deterioration in COVID-19 can basically be modeled according to the "kindling radical/bonfire hypothesis", where upstream radicals like superoxide sequentially trigger the downstream formation of even more reactive and deadly hydroxyl radicals.
Many diseases and drug-induced complications are associated with – or even caused by – an imbalance between the formation of reactive oxygen and nitrogen species (RONS) and antioxidant enzymes...
link.springer.com
Explore millions of resources from scholarly journals, books, newspapers, videos and more, on the ProQuest Platform.
www.proquest.com
COVID-19 is fundamentally an oxidative stress disease. The treatment is antioxidants.
