Ascorbic acid (vitamin C) is a water-soluble vitamin and the physiological function of this compound is largely related to its oxidation-reduction property. Vitamin C reduces vascular oxidative stress [12], and ameliorates the impairment in endothelium-dependent relaxation induced by hypercholesterolemia [13], hypertension [14], coronary artery disease [15], and chronic ethanol consumption [16]. In addition to its well known free radical scavenging property, vitamin C also influences the vascular redox state by directly stimulating the activity of the enzyme nitric oxide synthase (NOS), resulting in increased NO synthesis and vascular relaxation [14]. Vitamin C was also described to modulate enzyme systems that generate O2- and to increase superoxide dismutase (SOD) activity [12]. Based on the above-mentioned observations, we hypothesized that the impairment of endothelium-dependent relaxation, associated with a single dose of ethanol, is dependent on ROS generation. Thus, the aim of the present study was to investigate the role of oxidative stress on the endothelial dysfunction induced by acute ethanol intake. Vitamin C was chosen as an antioxidant since it has been describe to decrease ROS generation and to reduce oxidative stress in the vasculature.