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Year : 2021  |  Volume : 9  |  Issue : 2  |  Page : 61-67

Brain response to intraperitoneal and oral administration of monosodium glutamate in wistar rats

Department of Biochemistry, Faculty of Basic Medical Sciences, University of Calabar, Calabar P.M.B 1115 Cross River State, Nigeria

Correspondence Address:
Dr. Uche Stephen Akataobi
Department of Biochemistry, Faculty of Basic Medical Sciences, University of Calabar, P.M.B. 1115, Calabar, Cross River State
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/njecp.njecp_38_20

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Background: It has been reported that at high concentration monosodium glutamate (MSG) administration induces neurological toxicity caused by increased concentration of glutamate that promotes the production of free radicals and apoptosis. The blood–brain barrier is used by the brain to protect itself against the effect of glutamate and other neurotoxins but its level of protection varies with age. Aim and Objective: In this present study, we examined brain responses to combined intraperitoneal and oral administration of MSG at different doses in Wistar rats. Material and Method: 4 mg/g MSG was administered intraperitoneally to neonates in postnatal days 2, 4, 6, 8, and 10–2 groups and one of the groups was further administered 10 mg/g MSG orally as adult, while the last group received 10 mg/g MSG as adults only for 21 days. At the end of the 21 days, brain tissue was collected and used to determine MSG effect. Results: In the brain tissue, MSG administration caused a significant increase (P < 0.05) in glutamate decarboxylase, glutamate synthase, catalase, and glutathione peroxydase activities in a concentration dependent manner higher in group that received MSG both in neonate and adult. Superoxide dismutase also showed a significant increase (P < 0.05) in the treated groups but higher in group administered as neonates only. Conclusion: The result showed that MSG administration increased the level of neurotransmitters in both neonate and adult groups similarly and in response the brain increase the activity of the respective catabolic enzyme to protect itself against its effect

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