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        Monosodium glutamate induces memory and hepatic dysfunctions in mice: ameliorative role of Jobelyn® through the augmentation of cellular antioxidant defense machineries

        Omogbiya Adrian Itivere,Ben-Azu Benneth,Eduviere Anthony Taghogho,Eneni Aya-Ebi Okubo,Nwokoye Prisilla O.,Ajayi Abayomi Mayowa,Umukoro Solomon 한국독성학회 2021 Toxicological Research Vol.37 No.3

        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.

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        Datura metel stramonium exacerbates behavioral deficits, medial prefrontal cortex, and hippocampal neurotoxicity in mice via redox imbalance

        Vincent Onoriode Igben,Wilson Josiah Iju,Omogbiya Adrian Itivere,John Chukwuma Oyem,Peter Sunday Akpulu,Efe Endurance Ahama 한국실험동물학회 2023 Laboratory Animal Research Vol.39 No.2

        Background: Datura metel (DM) stramonium is a medicinal plant often abused by Nigerians due to its psychostimulatory properties. Hallucinations, confusion, agitation, aggressiveness, anxiety, and restlessness are reported amongst DM users. Earlier studies suggest that DM induces neurotoxicity and affect brain physiology. However, the exact neurological effects of DM extract in the medial prefrontal cortex (mPFC) and hippocampal morphology have not been elucidated. In this study, we evaluated the hypothesis that oral exposure to DM extract exerts a neurotoxic effect by increasing oxidative stress in the mPFC and the hippocampus and induces behavioral deficits in mice. Results: DM methanolic extract exposure significantly increased MDA and NO levels and reduced SOD, GSH, GPx and CAT activities in mice brains. In addition, our results showed that DM exposure produced cognitive deficits, anxiety, and depressive-like behaviour in mice following oral exposure for 28 days. Moreover, the mPFC and hippocampus showed neurodegenerative features, loss of dendritic and axonal arborization, a dose-dependent decrease in neuronal cell bodies’ length, width, area, and perimeter, and a dose-dependent increase in the distance between neuronal cell bodies. Conclusions: Oral exposure to DM in mice induces behavioural deficits, mPFC and hippocampal neuronal degenerations via redox imbalance in the brain of mice. These observations confirm the neurotoxicity of DM extracts and raises concerns on the safety and potential adverse effects of DM in humans.

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