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Long-term ethyl alcohol consumption induces a deficiency of essential nutrient thiamine (vitamin B 1 ) and profoundly impairs metabolic processes in nervous tissue, resulting in structural and functional alterations in the central nervous system (CNS). This study was performed to evaluate protective effects of thiamine acute dose on the level of glial fibrillary acidic protein (GFAP), a sensitive marker of astroglia, and B 1 -related enzyme thiamine pyrophosphokinase (TPK) activity in brain of rats chronically exposed to ethanol. The rats were divided into three groups as follows: i) control group; ii) rats given 15% ethanol solution as drinking water for 9 months (EtOH group), iii) EtOH rats given thiamine per os in a dose of 2.0 mg/kg one day before experiment termination (n = 4 in each group). GFAP levels were analyzed in cerebellum, brain cortex and hippocampus by western blot and immunohistochemistry. Brain TPK activity was measured with the use of the yeast apopyruvate decarboxylase apoenzyme (apoPDC). Thiamine concentration in liver was estimated with the use of thiochrome method. It was demonstrated that GFAP content was dramatically reduced in all studied brain regions of EtOH-exposed rats (approximately by 60%, P < 0.05) compared with control rats indicating profound astroglial dysfunction. Thiamine treatment was shown to recover GFAP levels up to 80% vs. control value in the brain of EtOH-exposed rats (P < 0.05). Ethanol consumption resulted in 3.7-fold decrease in liver thiamine content and 1.4-fold decrease in brain TPK activity, as compared with control (P < 0.05). Thiamine treatment of EtOH-exposed rats significantly elevated B 1 liver level, however, had no effect on brain TPK activity. Our data suggest that thiamine deficit can play an important role in alcohol-induced damage to brain astroglia. It is emerged that high-dose thiamine administration can represent effective treatment option against chronic effects of ethanol impact on brain structures. K e y w o r d s: chronic ethanol consumption, astrocytes, glial fibrillary acidic protein (GFAP), thiamine (vi-tamin B 1 ) deficit. E thyl alcohol is the most used toxicant worldwide. In 2012, over three million deaths were attributed to alcohol consumption, corresponding to 5.9% of the global total or one in every twenty deaths. In addition, 5.1% of the global burden of disease and injury, as measured in disability-adjusted life years, were attributable to alcohol abuse [1]. It is well known that one of the manifestations of alcohol-induced encephalopathy is thiamine (vitamin В 1 ) deficiency. Thiamine is a water-soluble vitamin, essential nutrition factor for humans and mammals. Thiamine deficiency (TD) accompanies almost all of known neurodegenerative diseases, including Wernike-Korsakoff syndrome (WKS), Leigh disease, Alzheimer disease, etc. TD is the critical factor in Wernicke-Korsakoff syndrome development in humans affected by chronic alcoholism [2, 3]. It has been estimated that approximately 80% of alcoholics express TD [4], which if left un...