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Moshood Abiola Folawiyo1 
, Modinat Adebukola Adefisayo2 , Omosola Fisayo Anifowose3 , Timilehin Micheal Oni *4 , Ayodeji Folorunsho Ajayi5
, Modinat Adebukola Adefisayo2 , Omosola Fisayo Anifowose3 , Timilehin Micheal Oni *4 , Ayodeji Folorunsho Ajayi5
1- Department of Physiology, Faculty of Basic Medical Sciences, Ekiti State University, Ado-Ekiti, Nigeria.
2- Federal University of Technology, Akure, Nigeria.
3- Ekiti State University, Ado-Ekiti, Ekiti State, Nigeria.
4- Ekiti State University, Ado-Ekiti, Ekiti State, Nigeria. ,onitimilehin48@gmail.com
5- Ladoke Akintola University of Technology, Ogbomosho, Nigeria.
2- Federal University of Technology, Akure, Nigeria.
3- Ekiti State University, Ado-Ekiti, Ekiti State, Nigeria.
4- Ekiti State University, Ado-Ekiti, Ekiti State, Nigeria. ,
5- Ladoke Akintola University of Technology, Ogbomosho, Nigeria.
Abstract: (20 Views)
Background: Monosodium Glutamate (MSG) is a flavour intensifier extensively used in the food industry; however, compelling scientific evidence has linked MSG to neurotoxicity.
Aim: The present study aimed to investigate whether camel milk (CM) could suppress neurotoxicity caused by MSG in Wistar rats.
Methods: Rats were grouped randomly (n=6 rats) into control, MSG (6 g/kg/day), MSG+CM (5 ml/kg/day after 15 minutes of MSG), and Recovery (MSG for the first 21 days, then left for another 21 days without any administration). All administrations were done orally for 21 consecutive days.
Results: Exposure to MSG led to a drastic reduction in brain and body weight. It markedly reduced the activities of catalase, superoxide dismutase (SOD), glutathione peroxidase (GPX), and the levels of glutathione (GSH) in the brain. In contrast, pro-inflammatory cytokines, such as Interleukin-1β (IL-1β), Tumour Necrosis Factor-α (TNF-α), Myeloperoxidase, Nitric oxide (NO), and C-reactive protein (CRP), Nuclear factor kappa B (NF-κb), caspase-3, and lipid peroxidation, as demonstrated by the MDA level, were prominently increased. The brain functional marker acetylcholinesterase was significantly upregulated, and dopamine activity was prominently reduced. In contrast, CM supplementation attenuated the weight and biochemical changes.
Conclusions: Camel milk supplementation demonstrates a therapeutic effect by alleviating MSG- induced neurotoxicity via antioxidant, anti-inflammatory, and anti-apoptotic mechanisms. The findings suggest that CM can be a potent dietary strategy to mitigate the neurotoxic side effects of MSG.
Aim: The present study aimed to investigate whether camel milk (CM) could suppress neurotoxicity caused by MSG in Wistar rats.
Methods: Rats were grouped randomly (n=6 rats) into control, MSG (6 g/kg/day), MSG+CM (5 ml/kg/day after 15 minutes of MSG), and Recovery (MSG for the first 21 days, then left for another 21 days without any administration). All administrations were done orally for 21 consecutive days.
Results: Exposure to MSG led to a drastic reduction in brain and body weight. It markedly reduced the activities of catalase, superoxide dismutase (SOD), glutathione peroxidase (GPX), and the levels of glutathione (GSH) in the brain. In contrast, pro-inflammatory cytokines, such as Interleukin-1β (IL-1β), Tumour Necrosis Factor-α (TNF-α), Myeloperoxidase, Nitric oxide (NO), and C-reactive protein (CRP), Nuclear factor kappa B (NF-κb), caspase-3, and lipid peroxidation, as demonstrated by the MDA level, were prominently increased. The brain functional marker acetylcholinesterase was significantly upregulated, and dopamine activity was prominently reduced. In contrast, CM supplementation attenuated the weight and biochemical changes.
Conclusions: Camel milk supplementation demonstrates a therapeutic effect by alleviating MSG- induced neurotoxicity via antioxidant, anti-inflammatory, and anti-apoptotic mechanisms. The findings suggest that CM can be a potent dietary strategy to mitigate the neurotoxic side effects of MSG.
Keywords: Camel milk (CM), Inflammation, Monosodium glutamate (MSG), Neurotoxicity, Oxidative stress
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The Iranian Journal of Toxicology
Arak University of Medical Sciences in collaboration with the Iranian Society of Toxicology
Website: http://ijt.arakmu.ac.ir
Email: tox.journal@gmail.com
