Thiamine Deficiency Induced Dietary Disparity Promotes Oxidative Stress and Neurodegeneration

Thiamine or vitamin B1 is a well known coenzyme and nutrient necessary for the assembly and right functioning of several enzymes involved in the energy metabolism. The present study evaluates oxidative stress and prevalence of neurodegenerative conditions in the brain following TD. The study was carried out on mice (Musmusculus) in three groups, namely control and thiamine-deficient group for 8 (TD 8) and 10 (TD 10) days. Lipid peroxidation was determined in terms of reduced glutathione (GSH) and thiobarbituric acid reactive substance (TBARS). The level of antioxidant enzymes such as catalase (CAT), glutathione reductase, glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione transferase (GST) were measured along with histopathological studies in all the groups. There was significant increase in the TBARS levels in group II (TD 8) and group III (TD 10) animals in comparison to controls (Group I). The GSH levels were found to be lower in both the treated groups. The level of antioxidant enzymes CAT (p < 0.001), glutathione reductase (p < 0.001), GPx (p < 0.001), SOD (p < 0.0001) were found to be significantly reduced in group III (TD 10) in comparison to controls. Histopathological studies showed moderated to extensive neuronal loss in group II and group III in comparison to control group. The increase in LPO and reduction in enzymes CAT, glutathione reductase, GPx, SOD, and GST following TD suggests mitochondrial dysfunction, neuronal loss acute oxidative stress that may impair the functioning of the brain along with the rise of neurodegenerative conditions in the affected animals.