*Corresponding author:Bruce K Kowiatek, the Wellness Pharmacy, 2228-E Papermill Rd, Winchester, VA 22601, 110 Highpointe Ct, Winchester, USA
Received: November 01, 2018; Published: November 20, 2018
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Administration of supplemental folic acid addresses the impaired DNA synthesis causing megaloblastic anemia; however, despite the possibility of high doses of folic acid -5 to 15 milligrams (mg) daily for up to four months -the extremely rapid initial onset of action -30 to 60 minutes -when administered orally is not in keeping with the accepted mechanism, which can take up to nearly 22 hours, even under enzymatic control. This would suggest an additional, complementary non-enzymatic mechanism of nucleotide methylation at work; it is, therefore, proposed here, with in vitro evidence put forth, that rapid, non-enzymatic methylation by folic acid, via 5,10-methylenetetrahydrofolate and 7,8-tetrahydrofolate intermediates, of deoxyuridine monophosphate to form thymidylate using the cell membrane phospholipid phosphatidylcholine as a methyl donor, leaving de-methylated phosphatidylethanolamine, is a viable additional and complementary mechanism in helping reduce megaloblastic red blood cells to normal size and function.
Keywords : Folic Acid; DNA; Megaloblastic Anemia; Deoxyuridine Monophosphate; Thymidylate
Abbreviations : PC: Phosphatidylcholine; DUMP: Deoxyuridine 5′-Monophosphate; DHFR: Dihydrofolate Reductase; THF: Tetrahydrofolate; dTMP: Deoxythymidine 5′-Monophosphate; SAM-e: S-Adenosylmethionine; PE: Phosphatidylethanolamine; TMS: Trimethylsilyl; PCCA: Professional Compounding Centers of America; NS: Normal Saline; HCL: Hydrochloric AcidIntroduction| Experimental| Results and Discussion| Acknowledgement| References|