Neurobehavioural Deficits, Atherogenic Risk, and Oxido-inflammatory Response in Mice Fed with Combined Sodium Benzoate and Monosodium Glutamate Supplementation in Normal and High-fat Diets

Abstract

Introduction/Background: The overuse of food additives and preservatives has become a source of concern globally due to the inherent risks associated with them. This study evaluated neurobehavioral performance, atherogenic risk, and oxido-inflammatory response in mice fed with normal and high-fat diets supplemented with combined sodium benzoate (SB) and monosodium glutamate (MSG). Materials/Methods: Mice were divided into four groups (n=6) and fed with normal diet (ND), high-fat diet (HFD), ND+MSG+SB, and HFD + MSG +SB, respectively, for 28 days. Neurobehavioral performance in mice was carried out in an open field, and Y-maze tests were performed. Serum was obtained to determine lipid profile and atherogenic risk, while brain homogenate was used to determine oxidative stress, inflammatory markers, and neurotransmitter-related enzyme activities. Results: This study reported that in mice fed with HFD, ND+MSG+SB, and HFD + MSG +SB, there was a significant (p < 0.05) decrease in explorative activity, an increase in anxiety-like behavior, as well as decreased memory performance. Malondialdehyde and nitrites levels increased, while levels of reduced glutathione and antioxidant enzyme activities, catalase and superoxide dismutase, were significantly reduced. Pro-inflammatory cytokines (TNF-α and IL-6) were significantly increased in the brains of mice fed with HFD, ND+MSG+SB, and HFD + MSG +SB when compared with control. Moreover, the activities of acetylcholinesterase increased while glutamic acid decarboxylase decreased significantly. Conclusion: In conclusion, SB and MSG supplementation in diets caused neurobehavioral deficits in mice, increased atherogenic risk, and upregulated oxidative stress and inflammatory response in mice brains.