The article demonstrates the dangerousness of graphene oxide, its toxicity, and the destabilizing effects of REDOX equilibrium, which cause cell death.
Researchers analyse the risks and toxicity of graphene oxide, which interferes with the normal functioning of mitochondria (cellular organelles responsible for supplying energy to cells).
The adverse biological effects were tested on cultured SH-SY5Y cells.
SH-SY5Y cells are human-derived cell lines used to study brain cells and neurodegenerative diseases because they are very similar to SK-N-SH neuroblasts, the embryonic cells of neurons.
One of the main conclusions of the study can be read in the abstract of the article : “We found that ultrasonic treatment changed the oxidation state and surface reactivity on the flat surface of GO (graphene oxide) due to its hydration activity, which caused peroxidation. of lipids and damage to the cell membrane“.
The article points out that the application of ultrasound can lead to the destruction of the primary structure of graphene oxide nanomaterials, “producing fragmentation and defects on the surface or edges, and affecting their behavior in the biological system“.
According to the authors, ultrasound generates “mismatched free radical electrons” that react by causing cells to oxidise, leading to a REDOX (oxidative stress) imbalance, causing DNA damage and generating ROS (reactive oxygen species, i.e. oxygen ion free radicals and peroxides).
This process is responsible for the toxicological effects of graphene oxide.
When the concentration of graphene oxide is higher than 40 μg/ml (40 micrograms per millilitre), cell survival is significantly reduced to less than 66% after 3 hours.
Apoptotic cell death was confirmed in the experiments, see Figure 1.
Fig. 1. Graphene oxide cell survival assay
The article focuses on cellular REDOX imbalance resulting from unbalanced antioxidant systems.
t was found that cells treated with GO graphene oxide induced excessive ROS production, which was the precursor of cellular oxidative stress.
To confirm this, the researchers used NAC (N-acetylCysteine) treatments, which reduced ROS levels and confirmed that GO graphene oxide was responsible for activating the NOX2 (oxidase) pathway, which is responsible for the REDOX imbalance.
In the authors’ own words, graphene oxide is responsible for “weakened antioxidant capacity“.
Therefore, it is confirmed that NAC (N-AcetylCysteine) is an effective antioxidant to counteract the REDOX imbalance caused by graphene oxide GO.
Among the conclusions, the following is revealing : “exposure to GO induced an alkalizing effect in lysosomes, affecting the normal progression of autophagy flux and limiting the clearance of autophagosomes, which ultimately resulted in excessive accumulation of autophagy-related substrates, including dysfunctional mitochondria.
Taken together, these toxic effects triggered mitochondria-mediated apoptotic cell death“.
Figure 2 shows how the whole process leading to cell death is initiated.
Note how the initial agents are GO graphene oxide nanosheets.
This process is called “disruption of mitochondrial homeostasis“.
Fig 2. : Oxidation process and cell death
Final Reflections
The article demonstrates the dangerousness of graphene oxide, its toxicity and the destabilising effects on the REDOX balance, causing cell death.
This confirms all the consequences and symptoms described in the symptoms of the so-called Acute Radiation Syndrome, or SARS-COV2.
Moreover, as all so-called “vaccines” contain graphene oxide, this substance can cause very serious health problems in the long term for those inoculated.
Therefore, it seems advisable to always have some reserves of NAC (N-AcetylCysteine) and antioxidants in the body to protect oneself from GO graphene oxide, especially if some of the classic symptoms of SARS COV-2 are noticed, in order to prevent the oxidation processes described by the researchers.
See (Alamdari, DH; Moghaddam, AB; Amini, S .; Keramati, MR; Zarmehri, AM; Alamdari, AH; Koliakos, G. 2020 | De Flora, S.; Balansky, R .; La Maestra, S. 2020 | Ibrahim, H.; Perl, A.; Smith, D.; Lewis, T. ; Kon, Z.; Goldenberg, R.; Williams, M. 2020 | Liu, Y.; Wang, M.; Luo, G. ; Qian, X.; Wu, C.; Zhang, Y.; Tang, Y. 2020 | Poe, FL; Corn, J. 2020 | Puyo, C.; Kreig, D.; Saddi, V.; Ansari, E .; Principe, O. 2020).
Bibliography
1.Alamdari, DH; Moghaddam, AB; Amini, S.; Keramati, MR; Zarmehri, AM; Alamdari, AH; Koliakos, G. (2020). Application of methylene blue-vitamin C–N-acetyl cysteine for treatment of critically ill COVID-19 patients, report of a phase-I clinical trial. European journal of pharmacology, 885, 173494. https://doi.org/10.1016/j.ejphar.2020.173494<2.
2.De Flora, S.; Balansky, R.; La Maestra, S. (2020) Rationale for the use of N‐acetylcysteine in both prevention and adjuvant therapy of COVID‐19. The FASEB journal, 34 (10), pp. 13185-13193. https://doi.org/10.1096/fj.202001807
3.Ibrahim, H.; Perla, A.; Smith, D.; Lewis, T.; Kon, Z.; Goldenberg, R.; Williams, M. (2020). Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous N-acetylcysteine. Clinical Immunology, 219, 108544.https://doi.org/10.1016/j.clim.2020.108544
4.Liu, Y.; Wang, M.; Luo, G.; Qian, X.; Wu, C.; Zhang, Y.; Tang, Y. (2020). Experience of N-acetylcysteine airway management in the successful treatment of one case of critical condition with COVID-19: a case report. Medicine, 99 (42).https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7571913/
5.Poe, Florida; Mais, J. (2020) N-Acetylcysteine: A potential therapeutic agent for SARS-CoV-2. Medical hypotheses, 143, 109862. https://doi.org/10.1016/j.mehy.2020.109862
6.Puyo, C.; Kreig, D.; Saddi, V.; Ansari, E.; Principe, O. (2020). Case report: Use of hydroxychloroquine and N-acetylcysteine for treatment of a COVID-19 positive patient. F1000Research, 9 (491), 491.
