To put it in very simple terms, I think what is going on is the graphene oxide, once it is in your system and blood, is causing the iron in your blood to collect (magnetically/electro magnetically ((cardio)) with the graphene oxide and the iron oxides are collecting together and causing the blood clots and micro blood clots.
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I like it.
https://pubs.rsc.org/en/content/articlelanding/2019/NH/C8NH00318A#!divAbstract
“In this review, we will describe the journey of graphene oxide after injection into the bloodstream, from the initial interactions with plasma proteins to the formation of the “biomolecular corona”, and biodistribution.”
-—COULD NOT GET FULL TEXT
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3259226/
“In comparison, two studies reported biodistribution and toxicity of graphene oxides following intravenous injection in mice. At doses of 0.1 or 0.25 mg, no toxicity was observed; however, a dose of 0.4 mg induced granulomas in the lungs, liver, spleen, and kidney and was lethal in 4/9 of the mice 98. Zhang et al. 106 also noted deposition and retention in the lungs with production of lung injury, inflammation, and granuloma formation when delivered intravenously at a dose of 0.4 mg. Granulomas are also induced in the lungs of drug abusers following intravenous injection of drugs containing talc particles 86. In summary, GFNs designed for intravenous drug delivery have the potential for bioaccumulation and granuloma formation although these potential complications may be decreased by surface modifications to achieve selective tumor targeting and to promote biodegradation following drug delivery as discussed in Section 4.5 and in Kotchey et al. 63.”
-—RECENT REVIEW DOES NOT DISCUSS THROMBUS FORMATION
Graphene oxide (GO), the new two-dimensional carbon nanomaterial, is extensively investigated for potential biomedical applications. Thus, it is pertinent to critically evaluate its untoward effects on physiology of tissue systems including blood platelets, the cells responsible for maintenance of hemostasis and thrombus formation. Here we report for the first time that atomically thin GO sheets elicited strong aggregatory response in platelets through activation of Src kinases and release of calcium from intracellular stores. Compounding this, intravenous administration of GO was found to induce extensive pulmonary thromboembolism in mice. Prothrombotic character of GO was dependent on surface charge distribution as reduced GO (RGO) was significantly less effective in aggregating platelets. Our findings raise a concern on putative biomedical applications of GO in the form of diagnostic and therapeutic tools where its prothrombotic property should be carefully investigated.