Protective effect of vitamin C against the ethanol mediated toxic effects on human brain glial cells

J Nutr Biochem. 2003 Oct;14(10):606-13. doi: 10.1016/j.jnutbio.2003.07.003.


It is now known that chronic consumption of excessive amounts of alcohol is a major source of social and medical problems. Ethanol-mediated glial cell activation may lead to neuron damage in many ways, including the formation of free radicals and production of pro-inflammatory molecules. Vitamin C (vit-C) is an essential dietary nutrient required as a co-factor for many enzymes and a very efficient antioxidant, protecting cells against free radical-mediated damage. The objective of this study was to evaluate the protective effects of vit-C on glial cell activation and viability against ethanol-mediated toxicity. Human brain astrocyte cells (HA) were exposed to ethanol (0, 50, and 350 mmol/L) for 24 h. We found that glial cells incubated with different concentrations of vit-C increase their vit-C in a dose-dependent manner. HA incubated with 0, 50 or 350 mmol/L of ethanol for up to 24 h showed toxic effects that were proportional to the levels of ethanol in the medium, HA showed increased levels of heat shock protein (Hsp70). However, cells enriched with vit-C before being exposed to ethanol, were better protected against the alcohol-mediated toxicity than non-supplemented cells, and showed significantly lower concentrations of Hsp70. Ethanol also caused increased expression of cyclooxygenase-2 (COX-2) and synthesis of prostaglandin E2 (PGE2), which were reduced by vit-C. In summary, HA supplemented with vit-C were significantly more resistant to the ethanol-mediated toxic effects.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Ascorbic Acid / pharmacology*
  • Astrocytes / cytology
  • Astrocytes / drug effects
  • Brain / cytology
  • Brain / drug effects*
  • Brain / metabolism
  • Cells, Cultured
  • Cyclooxygenase 2
  • Dinoprostone / metabolism
  • Ethanol / toxicity*
  • HSP70 Heat-Shock Proteins / metabolism
  • Humans
  • Isoenzymes / metabolism
  • Membrane Proteins
  • Neuroglia / cytology
  • Neuroglia / drug effects*
  • Neuroglia / metabolism
  • Prostaglandin-Endoperoxide Synthases / metabolism


  • HSP70 Heat-Shock Proteins
  • Isoenzymes
  • Membrane Proteins
  • Ethanol
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
  • Dinoprostone
  • Ascorbic Acid