Ascorbic Acid: An Antioxidant and Much More

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 20 August 2024 | Viewed by 963

Special Issue Editor

Department of Biological Sciences, Wayne State University, Detroit, MI 48202, USA
Interests: cellular mechanisms of Parkinson's disease; mitochondrial function and aging; non-enzymatic redox reactions and oxidative stress

Special Issue Information

Dear Colleagues,

As a molecule, ascorbic acid is a remarkable antioxidant that scavenges free radicals and reactive oxygen species. As a co-substrate for a number of enzymes, ascorbic acid is also instrumental in signaling, gene expression, and cellular metabolism. It is required by enzymes synthesizing norephinephrine and peptide hormones, and it regulates the transcription factor subunit HIF1α (hypoxia-inducible factor 1α) and the TET (Ten-eleven-translocation) DNA demethylases. Of course, the collagen-synthesizing enzymes, prolyl and lysyl hydroxylase, need ascorbic acid to maintain activity; this deficiency causes scurvy, the condition from which ascorbic acid gets its name. Ascorbic acid has been the subject of controversial claims about its effectiveness in combatting diseases such as the common cold and cancer and about the value of consuming megadoses of the vitamin for optimum health. To address these controversies and to truly understand the role of ascorbic acid in human health, we need to take a broader view of its actions. It is my hope that this Special Issue will bring together articles connecting the chemistry of ascorbic acid with its subtle but wide-ranging biological effects. Your work is an important part of this discussion, and I hope you will be willing to contribute your perspective. We invite you to submit your latest research findings or a review article to this Special Issue on “Ascorbic Acid: An Antioxidant and Much More”.

Best regards,

Prof. Dr. David Njus
Guest Editor

Manuscript Submission Information

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Keywords

  • ascorbic acid
  • reactive oxygen species
  • vitamin C
  • epigenetic regulation
  • sympathetic signaling

Published Papers (1 paper)

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Research

15 pages, 4348 KiB  
Article
Multifaceted Effects of L-Cysteine, L-Ascorbic Acid, and Their Derivatives on the Viability and Melanin Synthesis of B16/F10 Cells under Different Conditions
by Joon Yong Choi, Jae Won Ha and Yong Chool Boo
Antioxidants 2024, 13(3), 330; https://doi.org/10.3390/antiox13030330 - 07 Mar 2024
Viewed by 688
Abstract
The total melanin synthesis in the skin depends on various melanogenic factors, including the number of viable melanocytes, the level of melanogenic enzymes per cell, and the reaction rate of the enzymes. The purpose of this study is to examine the effects of [...] Read more.
The total melanin synthesis in the skin depends on various melanogenic factors, including the number of viable melanocytes, the level of melanogenic enzymes per cell, and the reaction rate of the enzymes. The purpose of this study is to examine the effects of L-cysteine (L-Cys), L-ascorbic acid (L-AA), and their derivatives on the tyrosinase (TYR) activity and autoxidation of L-3,4-dihydroxyphenylalanine (L-DOPA) in vitro and the viability and melanin synthesis of B16/F10 cells under different conditions. L-Cysteinamide (C-NH2), glutathione (GSH), L-Cys, L-AA, and N-acetyl L-cysteine (NAC) inhibited the catalytic activity of TYR in vitro. L-AA, C-NH2, L-ascorbic acid 2-O-glucoside (AAG), and 3-O-ethyl L-ascorbic acid (EAA) inhibited the autoxidation of L-DOPA in vitro. L-DOPA exhibited cytotoxicity at 0.1 mM and higher concentrations, whereas L-tyrosine (L-Tyr) did not affect cell viability up to 3 mM. L-AA, magnesium L-ascorbyl 2-phosphate (MAP), and L-Cys attenuated the cell death induced by L-DOPA. C-NH2 decreased the intracellular melanin level at the basal state, whereas L-AA, MAP, and AAG conversely increased it. C-NH2 reduced the number of darkly pigmented cells via in situ L-DOPA staining, whereas L-AA, MAP, GSH, and AAG increased it. C-NH2 decreased the intracellular melanin level at the alpha-melanocyte-stimulating hormone (α-MSH)-stimulated state, while NAC and GSH increased it. L-AA and C-NH2 decreased the intracellular melanin level at the L-Tyr-stimulated state, but NAC and GSH increased it. L-Ascorbyl tetraisopalmitate (ATI) showed no or minor effects in most experiments. This study suggests that L-AA can either promote or inhibit the different melanogenic factors, and C-NH2 can inhibit the multiple melanogenic factors consistently. This study highlights the multifaceted properties of L-Cys, L-AA, and their derivatives that can direct their therapeutic applications in hyperpigmentation, hypopigmentation, or both disorders. Full article
(This article belongs to the Special Issue Ascorbic Acid: An Antioxidant and Much More)
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