Thread by @DrJackKruse

1. Peroxynitrite (ONOO−) is an oxidant produced by the reaction between nitric oxide (NO) and superoxide radicals (O2 − ). It is known to produce oxidative stress by virtue of LPO, methionine, and sulfhydryl group oxidation in proteins, antioxidant depletion, and DNA damage. Do you know that NO and superoxide are both made directly from light frequencies (EMF) in most cells? The most damaging EMF is not the sun but the one man has forced us to live under. LIGHT > food

2. nnEMF (hyper)activates L-Type Voltage Gated Calcium Channels in the cell causing an increase in intracellular calcium.
Increased calcium activates two enzymes, nNOS and eNOS, which are nitric oxide synthases
These nitric oxide synthases are calcium dependent and can't activate unless there is increased levels of calcium in the cell and when calcium levels increase so too do levels of nitric oxide.

Nitric oxide can work along two different pathways; one pathway is normal but the other pathway is pathophysiological.

on the pathophysiological (bad) pathway the elevated levels of nitric oxide combine with superoxide to form peroxynitrite.
peroxnitrite is a potent oxidant that causes oxidative stress. This stimulus is used to change the metabolic pathways a cell can use to operate safely. Peroxnitrite is a free radical. All free radicals have unpaired electrons and this makes them magneto-chemicals. All magneto chemicals control timing switches in cells. Those switches are all photoswitches. patreon.com/posts/decentra…

3. At 4 minutes 30 seconds he gets to this point: Listen from there.

4. The photoswitch proof: peroxynitrite has roles as
(1) peroxide
(2) Lewis base
(3) free radical generator.

Physiological levels of CO2 and exhaust gas from mitochondrial metabolism, can change the outcome of peroxynitrite reactions. This is a secondary way that cells can control the effects of peroxynitrite.

The second major ability of this chemical is how it forms chemicals that control protein folding and affect ubiquitin marking. This is a feature found in many of the diseases of chronic illness. This exposes how neurodegeneration is exploding under the power of the 1996 FCC law that has no controls for nnEMF.

Did you, or your experts know that the formation of protein 3-nitrotyrosine (NO2Tyr) by peroxynitrite-dependent and -independent mechanisms, is one of the hallmarks of the actions of •NO-derived oxidants in biological systems?

As a result of this magnetochemistry, tyrosine nitration impacts protein structure and function, tyrosine kinase signal transduction cascades and protein turnover. This affects neurodegeneration risk = BIDEN and it affects cancer generation = BIDEN's son

5. Why don't we measure these chemicals on labs and account for them? They are produced by light induced reactions so they are too fast to account for and they all act locally at very short time scales to affect local mitochondria in tissues. This means they are quite partitioned because of how the reaction is QUENCHED inside of cells. This implies that while they can lead to damage they also have a POSITIVE purpose in photoswitching to different metabolic pathways when a cell needs a change. Remeber that peroxynitrite — the product of the DIFFUSION-controlled reaction of nitric oxide with superoxide radical — is a short-lived oxidant species that it can be a potent inducer of cell death if it is not quenched. Melanin is its main quencher. Conditions in which the reaction products of peroxynitrite have been detected and in which pharmacological inhibition of its formation or its decomposition have been shown to be of benefit include vascular diseases, ischaemia–reperfusion injury, circulatory shock, inflammation, pain and neurodegeneration.

6. The biological chemistry of peroxynitrite is also highly pH-dependent (protons = H+ and D) and is dictated primarily by reactions with thiols, carbon dioxide and transition-metal centers.

Reaction of peroxynitrite and/or peroxynitrite-derived radicals (for example, carbonate and nitrogen dioxide radicals) with targets results in one- and two-electron oxidations and nitration. Diffusion of peroxynitrite through biomembranes can cause oxidative damage at one to two cell diameters from its site of formation.

The most advanced pharmacological strategies to attenuate the toxic effects of peroxynitrite involve its fast (k>1 × 10^6 M−1s−1) catalytic reduction to nitrite (NO2) or its isomerization to nitrate (NO3) by metalloporphyrins. This makes integumentary and endogenous melanin production CRITICAL in mammals.

What else protects cells? Manganese and iron metalloporphyrinic compounds have been shown to rapidly react with peroxynitrite and promote its decomposition in a catalytic fashion. I've written many times about the atom Mn and nnEMF. I have also written many times why I look at blood smears for nnEMF risks due to peroxynitrite excess. This is where porphyrins exist. There are more heme based quenchers in mitochondrial cytochromes as well.

Such compounds — including manganese (III) meso-tetrakis((N-ethyl) pyridynium-2-yl) l porphyrin (MnTE-2-PyP), manganese (III) tetrakis(N-N′-diethylimidazolium-2-yl)porphyrin (AEOL-10150) and FeCl tetrakis-2-(triethylene glycol monomethyl ether) pyridyl porphyrin (FP15) — attenuate peroxynitrite- This implies LIGHT can be used safely without significant risk for the therapy of cardiovascular, inflammatory and neurodegenerative diseases. This is the leading frontier of quantum biology and what my Medical Freedom Constitutional Amendment brings to the forefront in El Salvador.

7. I will remind you to get to peroxynitrite you have to have NO. What creates NO in cells? UV light does. Every living cell on Earth releases ultraweak UV biophotons.

8. Nitric oxide (NO) is an omnipresent intercellular messenger in all vertebrates, modulating blood flow, thrombosis, and their neural activity. The biological production of NO is also important for nonspecific host defense, but NO itself is unlikely directly to kill intracellular pathogens and tumors.

Although NO is often described as highly toxic and reactive, it is not. Inhaling low concentrations of gaseous NO is approved by the Food and Drug Administration for the treatment of persistent pulmonary hypertension of the newborn. I bet your experts did not know this. NO is a potent controller of blood pressure in MAMMALS. High blood pressure is a signal of CHRONIC DISEASE presence because NO is being shunted to peroxynitrite production.

9. JUST HOW SAFE IS NO? NO can be produced for 80 years by neurons in human brain without ANY overt toxicity.
Paradoxically, the production of the same molecule can become highly damaging to the same neurons within a few minutes during pathological challenges as occur after cerebral ischemia. How is this possible?
The reaction of NO with superoxide (O2•−) to form the much more powerful oxidant peroxynitrite (ONOO−) is a key element in resolving the contrasting roles of NO in physiology and pathology.

Neither superoxide nor NO is particularly toxic in vivo because there are efficient means to minimize their accumulation. MELANIN CONTROLS THIS ACCUMULATION. So do other enzymes. Superoxide is rapidly removed by high concentrations of scavenging enzymes called superoxide dismutases (SOD) with distinct isoenzymes located in the mitochondria, cytoplasm, and extracellular compartments. NO is rapidly removed by its rapid diffusion through tissues into red blood cells (why I do smears), where it is rapidly converted to nitrate by reaction with oxyhemoglobin.

This limits the biological half-life of NO in vivo to less than a second, whereas the concentrations of NO relevant for cellular signaling can persist in phosphate-buffered saline for an hour. However, when both superoxide and NO are synthesized within a few cell diameters of each other, they will combine spontaneously to form peroxynitrite by a diffusion-limited reaction. In essence, every time NO and superoxide collide, they form peroxynitrite. No enzyme is required to form peroxynitrite because no enzyme can possibly catalyze any reaction as fast. Cellular diffusion of superoxide, peroxynitrite, and hydroxyl radical within their estimated first half-lives. These circles indicate the extent to where the concentration of each species from a point source would decrease by 50%. The diffusion of peroxynitrite accounts for its rapid reaction with carbon dioxide and with intracellular thiols. Thiols are sulfur based chemicals. When things have their sulfur consumed they no longer remain WATER SOLUBLE in cells. This cause more collateral effects.

The diffusion distance for nitric oxide is calculated based on its half-life of 1 s in vivo, which results mostly from its diffusion into red blood cells. The diffusion distance for hydroxyl radical is about the same diameter as a small protein, or 10,000 times smaller than peroxynitrite. All of these estimates involve computer simulations due to their speed, but varying the estimated half-lives by 10-fold would only alter the diameters by the square root of 10 or by 3.2-fold. The speed of light in tissues determines reaction times of the photoswitch in cells.

10. Generally, the CENTRALIZED physiological literature is content with discussing NO as a physiological signaling agent without considering its complex and controversial chemistry. A lot of biology is masked in the fog of the nebulous description reactive nitrogen species. Many of the biological effects attributed to NO are in fact mediated by peroxynitrite. While requiring some knowledge of the underlying convoluted chemistry of free radicals and nitrogen oxides, recognition of these reactions in vivo will produce a deeper DECENTRALIZED understanding of the underlying biology and help resolve many puzzling controversies.

11. NO is efficiently removed by reacting with oxyhemoglobin to form nitrate, which prevents even the highest rates of NO synthesis from directly reacting with oxygen to form significant amounts of nitrogen dioxide. However, the simultaneous activation of superoxide synthesis along with NO will completely transform the biological actions of NO by forming peroxynitrite. Several enzyme complexes, such as NADPH oxidases (NADPHox) and xanthine oxidase, can be activated in many cellular systems to actively produce large amounts of superoxide.

12. Comparison of oxidant production by the reaction of nitric oxide with superoxide versus oxygen. Both reactions are generally given equal weight in centralized science literature, but this obscures the vast difference in oxidant productions because of the vast difference in rates. WHY?

Because the formation of peroxynitrite depends on the product of the concentration of nitric oxide and superoxide, the rate of formation is proportional to the area.

Left below: estimate of peroxynitrite formation in the cytosol if a cell produces 10 nM nitric oxide, sufficient to activate guanylate cyclase enough to cause at least 10% relaxation of vessels, using 0.1 nM superoxide as an estimate of the basal steady-state concentration of superoxide.

Right below: increase in peroxynitrite formation if the formation of superoxide production increased either 100-fold (yellow) or 1,000-fold (yellow-orange), increases that can reasonably occur with the activation of NADPH oxidase. Nitric oxide is shown to increase only 10-fold and could rise to ~1 μM in highly inflamed states.

Far right (orange square): proportional area of nitrogen dioxide formation from 100 nM nitric oxide reacting with oxygen (estimated to be 50 μM in cells), which is magnified 100-fold.

This rate is the faster rate occurring in hydrophobic membranes and would be 300-fold smaller in solution. Pathways that stimulate the synthesis of superoxide vastly increase oxidant production compared with the reaction of nitric oxide with oxygen.

13. Although peroxynitrite is a strong oxidant, it reacts at a relatively SLOW rate with most biological molecules. This tells us TIMING IS CONTROLLED BY THIS RADICAL.

With its reaction with carbon dioxide and other major reactions in cells taken into account, peroxynitrite can still diffuse quite far on a cellular scale. Peroxynitrite is able to traverse cell membranes in part through anion channels.

The contrast with hydroxyl radical is dramatic. Hydroxyl radical is formed by a rather slow reaction via the reaction of ferrous iron with hydrogen peroxide, but is so reactive that it can only diffuse about the diameter of a typical protein. In contrast, peroxynitrite is formed each time superoxide and NO collide, but reacts slowly enough to react more selectively throughout the cell. That makes the biological and pathological implications of peroxynitrite far more interesting in mitochondrial biochemical pathway selection because it can have more subtle and specific actions on cells. This is how biophoton spectra are dialed up and down to cause biochemistry to operate below the cell level. NO BLOCKS ATP production = it controls timing of energy flow in cells.

14. You have to know your history when it comes to NO. Observation is the key first step in decentralized science. The identification of NO as EDRF was greatly facilitated by the independent work of John Hibbs, who was investigating how macrophages kill cancer cells.

Hibbs found that different batches of fetal calf serum had widely varying effects on the tumoricidal activity of macrophages in vivo. He observed in the local slaughterhouse that calf serum at the time was prepared from blood collected in buckets and deduced that endotoxin from contaminating bacteria was responsible for activating the macrophages.

He also noticed that activated macrophages rapidly depleted the media of some nutrient necessary for their tumoricidal activity. By supplementing the depleted media with each component, he discovered that arginine was the major compound that could restore the tumoricidal activity of macrophages. He also showed that the macrophages were producing nitrite and nitrate by oxidizing arginine to citrulline, but did not make the connection that macrophages may be producing NO and peroxynitrite.

The production of NO by macrophages was established by Stuehr and Nathan and peroxynitrite by Ischiropoulos et al. He deduced that arginine derivatives might be useful inhibitors and discovered that methylarginine blocked the tumoricidal activity of macrophages.

Thus he provided the background for Moncada’s group to show that EDRF was synthesized from arginine and that methylarginine blocked its biological activity.

15. WHY IS nnEMF CAUSING NEURODEGENERATION TODAY? The brain has massive amounts of NO to make peroxynitrite to cause the protein misfolding and apoptosis that marks these diseases. How do I know?

I am a brain surgeon, not a food guru, and I was at the top of my class and I did not quit. I know food and lack of exercise is not behind ANY of those diseases. And RFK JR and Trump need me way more than I need them.

Why?

A major difficulty in the identification of EDRF is the fact that endothelium produces relatively small amounts and is not an abundant cell in vivo. But the identification of EDRF as NO made sense of many puzzling results in the brain literature for years during my training.

We knew where cGMP was known to be involved in many intracellular functions. Deguchi and Yoshioka painstakingly purified a low-molecular-weight compound from nervous tissue that was required to activate soluble guanylate cyclase and showed that it was unexpectedly arginine.

For many years, it had been recognized that the brain had all of the enzymes necessary to convert citrulline to arginine, but curiously lacked arginase that is necessary for the complete urea cycle to be functional. It turns out this was by design and not bug, in the brain.

Most neurosurgeons know the urea cycle was not functional in the brain (why many diseases are tied to uric acid/oxalate issues), genetic deficiencies in these enzymes often resulted in phenotypes with neurological defects. Garthwaite and coworkers eventually connected the dots and showed that under normal physiological conditions the brain produced ~20 times more NO than the entire vasculature. I never forgot this lesson. It also told me the brain's mitochondria has to produce massive amounts of biophotons that create UV light!

16. The Melanin Renovation Rx blog I wrote 20 years ago is based on Noether's theorem, which is the key missing piece. The theory states that every differentiable symmetry of the action of a physical system with conservative forces has a corresponding conservation law. The symmetry in the mammalian physical system is based on UV light. Time symmetry implies energy conservation. So, what happens to mammals when they lose energy? They lose time symmetry. When you lose energy and information you lose healthspan and you have a chronic disease. patreon.com/posts/quantum-…

17. If you want to reverse chronic disease like DJT , @RobertKennedyJr and @NicoleShanahan They would talk publically about the law they both read that I wrote and they would read this thread and realize that this BLOG is where the FIRST step in that journey begins. patreon.com/posts/melanin-…

@RobertKennedyJr @NicoleShanahan 18. END OF THE LESSON. Some of us are already changing the world and not waiting on the USA.