Ascorbic acid mediates acetylcholine receptor increase induced by brain extract on myogenic cells.
Extracts of fetal calf brain cause a 3- to 5-fold increase in acetylcholine receptors (AcChoR) on cultured myogenic L5 cells. Purification of the substance causing the major portion of this receptor increase has been completed. Ultraviolet spectral characteristics, nuclear magnetic resonance, mass spectra, and AcChoR induction by the active factor are the same as those of commercially available ascorbic acid. The biological activity of ascorbic acid is not mimicked by reducing agents with or without sulfhydryl groups. Compounds related to ascorbic acid were tested for their ability to induce AcChoR increases on L5 cells. D-Isoascorbic acid is the only substance with identical biological activity to ascorbic acid. Dehydroascorbic acid and ascorbic acid 2-O-sulfate also induce AcChoR increases but with lower specific activity. These data show that ascorbic acid can play a role in regulating AcChoR expression in myogenic tissue, and the presence of ascorbic acid in the purified fraction from fetal calf brain accounts for its ability to increase AcChoR in L5 cells.
D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology*; D001923:Brain Chemistry; D002038:Bungarotoxins / Q000378:metabolism; D002417:Cattle; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D005260:Female; D009682:Magnetic Resonance Spectroscopy; D013058:Mass Spectrometry; D011247:Pregnancy; D011950:Receptors, Cholinergic / Q000378:metabolism*; D014020:Tissue Extracts / Q000494:pharmacology*
D002038:Bungarotoxins; D011950:Receptors, Cholinergic; D014020:Tissue Extracts; D001205:Ascorbic Acid