Vitamin C prevents the endothelial dysfunction induced by acute ethanol intake

Life Sci. 2015 Nov 15;141:99-107. doi: 10.1016/j.lfs.2015.09.006. Epub 2015 Sep 18.


Aims: Investigate the effect of ascorbic acid (vitamin C) on the endothelial dysfunction induced by acute ethanol intake.

Main methods: Ethanol (1g/kg; p.o. gavage) effects were assessed within 30min in male Wistar rats.

Key findings: Ethanol intake decreased the endothelium-dependent relaxation induced by acetylcholine in the rat aorta and treatment with vitamin C (250mg/kg; p.o. gavage, 5days) prevented this response. Ethanol increased superoxide anion (O2(-)) generation and decreased aortic nitrate/nitrite levels and these responses were not prevented by vitamin C. Superoxide dismutase (SOD) and catalase (CAT) activities as well as hydrogen peroxide (H2O2) and reduced glutathione (GSH) levels were not affected by ethanol. RhoA translocation as well as the phosphorylation levels of protein kinase B (Akt), eNOS (Ser(1177) or Thr(495) residues), p38MAPK, SAPK/JNK and ERK1/2 was not affected by ethanol intake. Vitamin C increased SOD activity and phosphorylation of Akt, eNOS (Ser(1177) residue) and p38MAPK in aortas from both control and ethanol-treated rats. Incubation of aortas with tempol prevented ethanol-induced decrease in the relaxation induced by acetylcholine. Ethanol (50mM/1min) increased O2(-) generation in cultured aortic vascular smooth muscle cells (VSMC) and vitamin C did not prevent this response. In endothelial cells, vitamin C prevented the increase on ROS generation and the decrease in the cytosolic NO content induced by ethanol.

Significance: Our study provides novel evidence that vitamin C prevents the endothelial dysfunction induced by acute ethanol intake by a mechanism that involves reduced ROS generation and increased NO availability in endothelial cells.

Keywords: Endothelial dysfunction; Oxidative stress; Superoxide anion; Vitamin C.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / antagonists & inhibitors
  • Acetylcholine / pharmacology
  • Animals
  • Antioxidants / therapeutic use*
  • Aorta / drug effects
  • Ascorbic Acid / therapeutic use*
  • Catalase / metabolism
  • Central Nervous System Depressants / antagonists & inhibitors*
  • Central Nervous System Depressants / toxicity*
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / metabolism
  • Ethanol / antagonists & inhibitors*
  • Ethanol / toxicity*
  • Glutathione / metabolism
  • In Vitro Techniques
  • Male
  • Nitric Oxide / metabolism
  • Phosphorylation
  • Protein Kinases / metabolism
  • Rats
  • Rats, Wistar
  • Reactive Oxygen Species / metabolism
  • Superoxide Dismutase / metabolism
  • Superoxides / metabolism
  • Vasodilator Agents / antagonists & inhibitors
  • Vasodilator Agents / pharmacology


  • Antioxidants
  • Central Nervous System Depressants
  • Reactive Oxygen Species
  • Vasodilator Agents
  • Superoxides
  • Nitric Oxide
  • Ethanol
  • Catalase
  • Superoxide Dismutase
  • Protein Kinases
  • Glutathione
  • Acetylcholine
  • Ascorbic Acid