Vitamin C Mitigating and Rescuing from Synergistic Toxicity: Sodium Fluoride, Silicofluorides, Aluminum Salts, Electromagnetic Pollution, and SARS-CoV-2

A supramolecular paradigm for mitigation and rescue from SARS-COV2 infection is proposed. Similarities between the Sanarelli-Shwartzman phenomenon and biological responses to viral pathogens are considered. Non-enzymatic group transfer catalysis (NGTC) by L-ascorbic acid, the L-ascorbic acid free radical and the 2-O-phosphate substituted L-ascorbic acid derivative are proposed under the ascorbolysis hypothesis to provide a supramolecular basis for mitigating the synergistic toxicity and catalytic mimicry by the environmental toxicants, sodium fluoride, aluminum salts, and silicofluorides in public water supplies. Ascorbolysis is the term we adopt to describe a redox active, hyperconjugated, vinylogous variant of acidolysis. The objective of this paper is to provide a plausible supramolecular basis for mitigation and rescue from well-known environmental toxicity represented by the presence of sodium fluoride, aluminum salts, and silicofluoride species in public water supplies. An overview of the conceptual basis for NGTC by vitamin C during inflammatory states is provided. Controversies concerning the initial oxidation steps and pH-dependent speciation of L-ascorbic acid are addressed. Non-skeletal fluorosis is a serious systemic malady which we propose arises from disruption of hydrogen bond networks and hydrogen bond cooperativity resulting from the marked electronegativity and hydrogen bond accepting ability of fluoride atoms found in NaF and AlFx species. AlFx species have been previously shown to arise in situ spontaneously from NaF, aluminum salts, and silicofluorides often found in toothpastes and “fluoridated” drinking water. AlFx species are thought to act as isosteric mimics of biophosphates during group transfers of phosphoryl moieties. We propose that catalytic mimicry by AlFx species inhibits postulated non-enzymatic kinase-like and RNA polymerase-like function of the AA-2P derivative during inflammatory states. We describe how NGTC by L-ascorbic acid is likely to be disrupted by AlFx and sodium fluoride of a specific H3-O2 intramolecular hydrogen bond in L-ascorbic acid, the L-ascorbic acid free radical, and their 2-O-substituted derivatives, which are necessary for NGTC in the moderately acidic, mildly oxidative, relatively hydrophobic microenvironment which typify inflammatory states. Suggestions are made to achieve less variation in results of large randomized clinical trials (RCTs) seeking to validate use of high-dose intravenous vitamin C in critical care and cancer settings.