Ascorbic acid leads to glycation and interferes with neurite outgrowth

Exp Gerontol. 2019 Mar:117:25-30. doi: 10.1016/j.exger.2018.08.005. Epub 2018 Aug 24.

Abstract

Ascorbic acid better known as vitamin C, is a reducing carbohydrate needed for a variety of functions in the human body. The most important characteristic of ascorbic acid is the ability to donate two electrons, predestining it as a major player in balancing the physiological redox state and as a necessary cofactor in multiple enzymatic hydroxylation processes. Ascorbic acid can be reversibly oxidized in two steps, leading to semidehydroascorbic acid and dehydroascorbic acid, respectively. Further degradation is irreversible and generates highly reactive carbonyl-intermediates. These intermediates are able to induce glycation of proteins, a non-enzymatic and unspecific reaction of carbonyls with amino groups involved to several age-related diseases. In this study, we investigated the effect of ascorbic acid- and dehydroascorbic acid-induced glycation on PC12 cells, which represent a model for neuronal plasticity. We found that both applications of ascorbic acid or dehydroascorbic acid leads to glycation of cellular proteins, but that ascorbic acid interferes more with viability and neurite outgrowth compared with dehydroascorbic acid.

MeSH terms

  • Animals
  • Ascorbic Acid / pharmacology*
  • Cell Survival / drug effects
  • Dehydroascorbic Acid / pharmacology
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Glycation End Products, Advanced / drug effects
  • MAP Kinase Signaling System / drug effects
  • Neuronal Outgrowth / drug effects*
  • PC12 Cells
  • Phosphorylation / drug effects
  • Rats

Substances

  • Glycation End Products, Advanced
  • Extracellular Signal-Regulated MAP Kinases
  • Ascorbic Acid
  • Dehydroascorbic Acid