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Ascorbic acid leads to glycation and interferes with neurite outgrowth
Jonas Scheffler1, Kaya Bork1, Veronika Bezold1
1Institut für Physiologische Chemie, Martin-Luther-Universität Halle-Wittenberg, Hollystr. 1, D-06114 Halle/Saale, Germany.
Experimental Gerontology
|August 28, 2018
Summary
Vitamin C (ascorbic acid) and its oxidized form, dehydroascorbic acid, can cause protein glycation. Ascorbic acid more significantly impacts cell viability and neurite outgrowth in neuronal models.
Area of Science:
- Biochemistry
- Cell Biology
- Neuroscience
Background:
- Ascorbic acid (vitamin C) is a vital reducing carbohydrate essential for human physiological functions.
- Its key role involves electron donation, maintaining redox balance, and acting as a cofactor in enzymatic hydroxylation.
- Oxidation of ascorbic acid yields semidehydroascorbic acid and dehydroascorbic acid, which can degrade into reactive carbonyl intermediates.
Purpose of the Study:
- To investigate the impact of ascorbic acid and dehydroascorbic acid-induced protein glycation.
- To examine these effects using PC12 cells as a model for neuronal plasticity.
Main Methods:
- Treatment of PC12 cells with ascorbic acid and dehydroascorbic acid.
- Assessment of cellular protein glycation.
- Evaluation of cell viability and neurite outgrowth.
Main Results:
- Both ascorbic acid and dehydroascorbic acid induced glycation of cellular proteins.
- Ascorbic acid demonstrated a more pronounced negative effect on PC12 cell viability compared to dehydroascorbic acid.
- Ascorbic acid also showed a greater interference with neurite outgrowth than dehydroascorbic acid.
Conclusions:
- Protein glycation by both ascorbic acid and dehydroascorbic acid occurs in neuronal models.
- Ascorbic acid poses a greater risk to neuronal viability and plasticity due to its more significant impact on these cellular processes.
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