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Dependence of Vitamin B1 Metabolism and the State of Astroglia in the Rat Brain on the Supply with this Vitamin

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Vitamin В1 deficiency was modeled in rats; their daily diet during 6 weeks contained about 20% of the necessary amount of thiamine. Under these conditions, the total content of vitamin В1 (thiamine) in the liver was, on average, 18.3% of the control, while the content of thiamine diphosphate (ТDP) in the blood and cerebral tissues was 40%. General indices of the redox balance (levels of reactive oxygen species, ROSs, and of free SH groups) were also smaller. The activity of thiamine pyrophosphokinase (TPK) in the brain homogenate of animals with thiamine deficiency (TD) was 35% higher than that in the control. In three cerebral structures, the cortex, cerebellum, and hippocampus, we measured the contents of proteins involved in thiamine metabolism, namely thiamine transporter (ТHTR) and TPK. In TD, directions of alterations of these indices for the above-mentioned proteins were opposite; the TPK content in all cerebral structures increased, while the THTR content in the cerebellum and hippocampus decreased. After single injections of 2.0 mg/kg thiamine into animals with TD 24 h before the completion of the experiment, the content of TPK in all cerebral structures increased. As to ТHТR, such effect was observed only in the cortex, while the reactions to thiamine injections in the cerebellum and hippocampus were not clearly manifested. We also estimated the content of glial fibrillary acidic protein (GFAP), an astrocyte marker, in all examined cerebral structures. In TD, this index was stably lower in all structures but returned to nearly control levels after single thiamine injection. Possible relations between alterations in the content of key proteins involved in thiamine metabolism and the supply of the organism with this vitamin are discussed.

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Pavlova, A.S., Stepanenko, S.P., Chekhovskaya, L.I. et al. Dependence of Vitamin B1 Metabolism and the State of Astroglia in the Rat Brain on the Supply with this Vitamin. Neurophysiology 48, 336–345 (2016). https://doi.org/10.1007/s11062-017-9607-0

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  • DOI: https://doi.org/10.1007/s11062-017-9607-0

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