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Background: Monosodium Glutamate (MSG) is one of the most commonly used flavorenhancing substances that may lead to neurological disorders. Objectives: The present work aimed to evaluate the role of L-ascorbic acid (AA) and -tocopherol (T) on the MSGinduced memory and neurobehavioral changes in rats. Methods: Thirty male Wistar albino rats were randomized into five equal groups: (1) control group, (2) MSG group received MSG (2mg/g BW) daily, (3) MSG+A group received MSG as in MSG group, and AA (100 mg/kg BW) daily, (4) MSG+T group received MSG as in MSG group, and T (600 mg/kg BW) twice weekly, and (5) MSG+AT group received MSG as in MSG group, AA as in MSG+A group, and T as in MSG+T group. After 3 weeks, neurobehavioral changes were assessed by open field test and Y maze. Oxidative stress markers were estimated, and immunohistochemistry was studied in hippocampal region. Results: MSG resulted in impairment of memory and induction of anxiety, with increased hippocampal malondialdehyde and decreased superoxide dismutase and glutathione peroxidase. Treatment with AA or T improved all the measured biochemical parameters, and the MSG-induced hippocampal degenerative changes, with decreased glial fibrillary acidic protein (GFAP) and synaptophysin expression. Combined administration of both vitamins was more effective in amelioration of MSG-induced impairments rather than taking AA or T alone. Conclusion: Both AA and T exhibit protective effects against neurobehavioral changes, oxidative stress and hippocampal degenerative changes induced by MSG toxicity, with more potent efficacy of their combination.

Background and Objectives: Hepatic steatosis has become the most common cause of chronic liver disease among children worldwide. Lipophagy has been considered as a pathway affecting steatosis development and progression. This study aimed to evaluate the immunohistochemical expression of Beclin1 and LC3A in pediatric hepatic tissues with steatosis and to correlate their expression with clinicopathological parameters. Methods This study included 81 Egyptian pediatric patients with hepatic steatosis. Also, 21 pediatric cases without hepatic steatosis were included. All specimens were stained by Beclin1 and LC3A antibodies. Results Higher beclin1 expression was significantly correlated with higher stages of fibrosis and distorted liver architecture in chronic liver diseases group, (P = 0.043) for both. The higher positivity, percentage and median values of H score of LC3A expression were seen in control group rather than in chronic liver disease group or the inborn error of metabolism group (P = 0.055, 0.001, 0.008 respectively). Higher positivity of LC3A was significantly associated with higher stages of fibrosis and distorted liver architecture in the studied inborn error of metabolism group (P = 0.021) for both. Conclusions Fluctuation of autophagy at different stages of pediatric hepatic steatosis and different disease etiology proved by different intensity grades of Beclin 1 and LC3A immunohistochemical expression.