Abstract

<p>Thiamine or vitamin B1 has an antioxidant property. It plays a vital role in energy metabolism as it is directly or indirectly involved in the metabolism of lipids, glucose, amino acids and neurotransmitters. Present study emphasizes the role of thiamine deficiency (TD) on the mitochondrial enzymes involved in energy metabolism and neurotransmission. The study was carried out on <em>Mus musculus</em> in three groups, namely control and thiamine-deficient group for 8 (TD 8, group II) and 10 (TD 10, group III) days. Activity of TCA cycle enzymes such as succinate dehydrogenase (SDH), malate dehydrogenase (MDH) and fumarase were measured along with the activity of enzyme acetylcholine esterase (Ach E) involved in the release of neurotransmitter. These biochemical changes were further correlated with histopathological changes in TD. A significant decrease in the enzymatic activity of SDH was found in group II (p<.05) and group III (p<.001) in comparison to the control group. Similarly a significant reduction in the enzymatic activity of MDH (<em>p</em> < 0.0001) in the TCA cycle was also found in group III (TD 10). Fumarase levels were also found to be low in both the treated groups in comparison to the control. Ach E activity was also found to be decreased in group II (p<.05) and group III (p<.001) in comparison to the control group. Histopathological analysis via transmission electron microscopy (TEM) showed neurodegenerative features in the brain of thiamine deficient mice. Diminished activity of mitochondrial enzymes and AchE suggests impairment in energy metabolism and disturbances in the release of neurotransmitter during TD. Pathological changes were also in conformity with the fact that TD impedes metabolism and it’s prolong impairments would further diminish brain functions. Our results suggest nutritional corrections with thiamine might lead to the improvement from neurological disorders or neurodegenerative conditions. </p>

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