z-logo
open-access-imgOpen Access
Monosodium glutamate induces memory and hepatic dysfunctions in mice: ameliorative role of Jobelyn® through the augmentation of cellular antioxidant defense machineries
Author(s) -
A.I. Omogbiya,
Benneth BenAzu,
Anthony T. Eduviere,
Aya-Ebi Okubo Eneni,
Prisilla O Nwokoye,
Abayomi Mayowa Ajayi,
Solomon Umukoro
Publication year - 2020
Publication title -
toxicological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.872
H-Index - 30
eISSN - 2234-2753
pISSN - 1976-8257
DOI - 10.1007/s43188-020-00068-9
Subject(s) - monosodium glutamate , antioxidant , malondialdehyde , neurotoxicity , saline , medicine , endocrinology , alkaline phosphatase , chemistry , oxidative stress , pharmacology , toxicity , enzyme , biochemistry
This study investigated the effect of high doses of monosodium glutamate (MSG), a known food additive on hepatic, memory and locomotor functions in mice, and the ameliorative potentials of Jobelyn ® (JB), a unique dietary supplement. Twenty four  male Swiss mice  divided into 4 groups (n = 6) were given MSG (2, 4 and 8 g/kg) or normal saline (10 mL/kg) orally for 14 days. In the intervention study, another set of 30 male Swiss mice distributed into 5 groups (n = 6) received normal saline, MSG (8 g/kg) alone or in combination with JB (5, 10 and 20 mg/kg) orally, for 14 days. Memory and locomotor functions as well as brain oxido-nitrergic stress biomarkers were then assessed in both studies. The hepatic oxido-nitrergic stress biomarkers, liver enzymes functions and histomorphology of the liver were also assessed. MSG (2, 4 and 8 g/kg) produced memory dysfunction, hyperlocomotion, increased malondialdehyde and nitrite levels accompanied by decreased antioxidant status in the brain and hepatic tissues. MSG-treated mice had increased hepatic enzyme activities (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) and distorted cyto-architectural integrity of the liver. These findings further suggest that MSG compromised hepatic functioning, which might also contribute to its neurotoxicity. However, JB (5, 10 and 20 mg/kg, p.o) attenuated the memory deficit, hyperlocomotion, increased oxido-nitrergic stress responses in the brain and hepatic tissues induced by MSG (8 g/kg, p.o). JB also normalized hepatic enzymes activities and histomorphological changes in MSG-treated mice. Taken together, JB mitigated MSG-induced toxicity through mechanisms relating to enhancement of cellular antioxidant-machineries and normalization of hepatic enzymatic functions.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here