Vitamin C prevents the endothelial dysfunction induced by acute ethanol intake

Author(s)

Hipolito, Ulisses V. ^{[1, 2]} ; Callera, Glaucia E. ^[3] ; Simplicio, Janaina A. ^{[1, 2]} ; De Martinis, Bruno S. ^[4] ; Touyz, Rhian M. ^[3] ; Tirapelli, Carlos R. ^[2]

Affiliation

^[1] Univ Sao Paulo, Fac Med Ribeirao Preto, Programa Posgrad Farmacol, BR-14040902 Ribeirao Preto, SP - Brazil

^[2] Univ Sao Paulo, Escola Enfermagem Ribeirao Preto, Dept Enfermagem Psiquiatr & Ciencias Humanas, Farmacol Lab, BR-14040902 Ribeirao Preto, SP - Brazil

^[3] Univ Ottawa, Kidney Res Ctr, Ottawa Hosp Res Inst, Ottawa, ON - Canada

^[4] Univ Sao Paulo, Fac Filosofia Ciencias & Letras Ribeirao Preto, BR-09500900 Sao Paulo - Brazil

• Document type: Journal article
• Source: Life Sciences; v. 141, p. 99-107, NOV 15 2015.
• Web of Science Citations: 8

Abstract

Aims: Investigate the effect of ascorbic acid (vitamin C) on the endothelial dysfunction induced by acute ethanol intake. Main methods: Ethanol (1 g/kg; p.o. gavage) effects were assessed within 30 min 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 (250 mg/kg; p.o. gavage, 5 days) prevented this response. Ethanol increased superoxide anion (O-2(-)) 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 (Ser1177 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 (50 mM/1 min) increased O-2(-) 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. (C) 2015 Elsevier Inc. All rights reserved. (AU)

• FAPESP's process: 10/05815-4 - Assessment of the role of angiotensin II in the cardiovascular effects induced by acute ethanol consumption
• Grantee: Carlos Renato Tirapelli
• Support Opportunities: Regular Research Grants
• FAPESP's process: 10/01383-2 - Participation of Oxigen Reactive Species in the Cardiovascular Dysfunctions Induced by Acute Ethanol Consumption
• Grantee: Ulisses Vilela Hipólito
• Support Opportunities: Scholarships in Brazil - Doctorate