Free fatty acids (FFA) and fatty acid ethyl esters (FAEE) were extracted from different organs of rats administered ethanol, which was found to have induced FAEE formation, which reached its highest levels in the heart, followed by kidney, brain and liver; the ethanol administration resulted also in a marked increase of total FFA content, particularly in brain, kidney, heart and liver. Pretreatment of animals with Metadoxine one hour before ethanol administration inhibited significantly both FAEE and FFA accumulation in all organs examined. These effects were concomitant with the decreased levels of ethanol in blood found in alcohol-intoxicated rats pretreated with Metadoxine. Our results point to the role of fatty acid ethyl esters as possible mediators in the production of alcohol-dependent syndromes, especially in organs lacking oxidative pathways. Administration of Metadoxine, through an increment in alcohol metabolism and turnover, greatly reduces this metabolic abnormality, warranting its potential usefulness as a pharmacological tool in alcoholism management.