Ingestion of elevated amounts of ethanol in humans and rodents induces hemorrhagic gastric lesions, at least in part by increasing oxidative stress. The present study was undertaken in order to evaluate the influence of a bicarbonate-alkaline mineral water (Uliveto^®) on ethanol-induced hemorrhagic gastric lesions in mice. Lesions were evaluated by both macroscopic and microscopic analysis. In a first set of experiments, mice were allowed to drink Uliveto^® or reference water ad libitum until 3 h prior to intragastric (i.g.) ethanol (23 ml/kg) administration. Neither Uliveto^® nor reference water did afford any protection. In a second set of experiments, acute exposure to reference water (35 ml/kg, i.g.), given 30 min before ethanol, did not inhibit gastric lesions. However, administration of the same amount of Uliveto^® caused a remarkable reduction in ethanol-evoked gastric lesions. Ethanol administration increased 4-hydroxy-2-nonenal levels, a byproduct of oxidative stress, in the luminal part of the gastric mucosa. This response was substantially reduced by about 70% by Uliveto^®, but not by reference water. Reference water, added with the bicarbonate content, present in the Uliveto^® water, protected against ethanol-induced lesions. Thus, acute pre-exposure to bicarbonate-alkaline mineral water (Uliveto^®) protects from both oxidative stress and hemorrhagic gastric lesions caused by ethanol. The elevated bicarbonate content of Uliveto^® likely accounts for the protection against ethanol-induced gastric injury.