In the case of SARS-CoV-2, the spike protein has been known to induce mitochondrial fragmentation. We are going to look the various mechanisms involved in mitochondrial degradation, and how both pathogenic cascades and electrically charged nanoparticles may be involved in apoptosis (cellular death).
Melatonin has a protective effects on the mitochondria, and some may be aware of the only substance capable of activating Cb1 receptors and the production of melatonin in the body, but that piece will be set aside for a later article 😋
Cytoplasm is between the cell membrane and the nucleus. mRNA comes out of the nucleus to induce the production of proteins. Endoplasmic reticulum (ER) surround the nucleus and is the receptor for nucleic mRNA. Some areas of ER have ribosomes. Mitochondria tends to surround ER as the center of energy production via ATP.
Mitochondria have their own DNA, ribosomes, RNA, and set of enzymes to perform their own action. Some of these mitochondrial products are exchanged into the Golgi Apparatus, which is the packaging area of the cell. Studies have found mitochondria to be especially effected by spike protein, whereas other structures are unaffected.
Within the mitochondria there is an additional electron transport chain, that allows aerobic respiration in the presence of oxygen. If the mitochondrial electron transport chain is “sped up”, the increase in activity will produce Reactive Oxygen Species (ROS). ROS may reach saturation and begin damaging the mitochondria and surrounding organelles, then spill outside of the cell in the case of apoptosis.
Genetics and Amyloids
Raman Spectroscopy has found normal mitochondrial DNA concentration to be 2.2mg/mL, whereas concentration of spike infected mitochondria was measured at 1.2mg/mL; a decrease of nearly 50%!
Normal RNA concentration is 2.25mg/mL, whereas concentration of spike infected mitochondria was measured at ~4mg/mL.
Normal Saccharide (Glucose and Pyruvate) concentration is 1.5mg/mL and found to be 0.7mg/mL in the presence of spike protein.
Spike protein causes a cascade that increases the production of ATP. The increase in ATP production necessarily causes the concentration of ROS to increase.
This would be evidence of not only the origin of ROS wreaking havoc in a paracrine fashion, but also of genetic dysregulation within the cell. Reminders of the MSH3 gene present at the Furin Cleavage Site of the S-1 subunit of the spike protein, is one known mechanism causing genetic repair dysregulation and posit the presence of this gene as a major factor in the discrepancy in nucleotide production.
If MSH2 forms a complimentary pair with MSH3, as it is known to do, then the MSH6 concentration would necessarily increase. An increase in MSH6 may in turn cause the increase of production of other genetic material in an attempt to return MSH6 concentration to “normal”.
The added piece of knowing an increase of saturated phospholipids may also be an indication of the early building blocks of what the body deposits later; observed as amyloidosis.
Cationic (Positive) Charges
In addition to known mechanisms behind spike mediated mitochondrial fragmentation, there is another vector of damage that may be overlooked by the presence of the spike protein, and that would be the effect cationic (positive) charges have inducing apoptosis via mitochondrial mediated apoptosis.
Central to gene therapy technology has been the use of cationic polymers as vectors for DNA and RNA (polyfectins). These have been presumed to be safer than viral systems which, for example, have been found to switch on oncogenes. Two key polycations that have been intensively researched for use as synthetic vectors are poly(ethylenimine) and poly(l-lysine). A frequent stumbling block with these polyfectins is that long-term gene expression in cell lines has not been achieved.
Recently it has transpired that both of these polycations can induce mitochondrially mediated apoptosis. It is the aim of this review to discuss the mechanisms behind the observed polycation toxicity including roles for little studied cellular organelles in the process such as the lysosome and endoplasmic reticulum.
Questions regarding the fate of free polymers in the cytoplasm, their interaction with other cellular organelles or the activity of those retained within the lysosome are of pivotal importance, as the cation organelle interaction may afford other routes to mitochondrially mediated apoptosis.
If a comparatively low molecular weight molecule containing amino groups such as gentamicin can cause lysosome destabilization and cathepsin release ultimately triggering the executioner caspases through the mitochondrion, what is going to be the effect of concentration of the smaller PEI once degraded within the lysosome and outside in the cytoplasm?
Signal Across Barriers
Concern has also been raised recently by a study which demonstrated that nanoparticles can induce DNA damage via signaling from across a cellular barrier.
Nanoparticles can damage human fibroblast cells across an intact cellular barrier without having to cross the barrier. The damage is mediated by a novel mechanism involving transmission of purine nucleotides (such as ATP) and intercellular signaling within the barrier through connexin gap junctions or hemichannels and pannexin channels.
The outcome, which includes DNA damage without significant cell death, is different from that observed in cells subjected to direct exposure to nanoparticles. Our results suggest the importance of indirect effects when evaluating the safety of nanoparticles.
Gap junctions form channels between adjacent cells. The core proteins of these channels are the connexins. Regulation of gap junction communication (GJC) can be modulated by connexin-associating proteins, such as regulatory protein phosphatases and protein kinases, of which c-Src is the best-studied.
Structural proteins, notably zona occludens-1 (ZO-1) and microtubules, have been found recently at gap junctions. Along with the expansion of the list of connexin-associating proteins, reports have appeared that suggest that connexins might have additional roles in addition to their channel function, such as transcriptional and cytoskeletal regulation.
Microtubules and Orch-OR
The damage is mediated by a novel mechanism involving transmission of purine nucleotides and microtubules.
When operating at the quantum scale of biology, technology must account for the consequences of imposing a positive charge to individual organelles, as well as the transcriptional and cytoskeletal consequences present; not only within the targeted theoretical pharmacokinetics, but the consequences across “cellular barriers”; both within and without the cell itself.
The only framework I am currently aware of capable of contemplating the implications of the physics of biology on the quantum scale would be Stuart Hammeroff, and 2 time Nobel Laureate for Physics, Roger Penrose’ ORCH-OR Theory.
Whereas Orch-OR Theory ultimate failed in its claim as a “theory of consciousness”, its biological observations have since proven to be correct. The ability to signal across a barrier may be done in an electro-mechanical fashion via necessary cascading of dipoles manifesting the structure of microtubules.
Polarity, Transcription, & Spike
If a single electron is present, it will necessarily cause “polarity flips” in naturally negatively primed cytoplasm and organelles, via the microtubule structure. If the electrophysical structure of microtubules is impeded, then its ability to naturally transcribe genetic information, both nucleic and mitochondrial, will cause interference in the fidelity of how the genetic information is transcribed.
When genetic information is unable to be transcribed correctly, then the “cell” will signal cancerous and may move to apoptosis. The pathophysiological cascade spike is observed inducing may not be exclusive to its biology. However, spike’s biology may be used as an exclusive scapegoat to deflect from other known pathologies of mitochondrial apoptosis to be induced by “the technology of future” alone…
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