Sodium benzoate induces neurobehavioral deficits and brain oxido-inflammatory stress in male Wistar rats: Ameliorative role of ascorbic acid.

Autor: Asejeje FO; Department of Chemical Sciences, Faculty of Natural Sciences, Ajayi Crowther University, Oyo, Nigeria., Ajayi BO; Department of Chemical Sciences, Faculty of Natural Sciences, Ajayi Crowther University, Oyo, Nigeria., Abiola MA; Department of Biochemistry, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Nigeria., Samuel O; Department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Nigeria., Asejeje GI; Department of Chemistry, Faculty of Science, University of Ibadan, Ibadan, Nigeria., Ajiboye EO; Department of Physiology and Anatomy, Faculty of Basic Medical Sciences, Ajayi Crowther University, Oyo, Nigeria., Ajayi AM; Department of Pharmacology and Therapeutics, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Nigeria.
Jazyk: angličtina
Zdroj: Journal of biochemical and molecular toxicology [J Biochem Mol Toxicol] 2022 May; Vol. 36 (5), pp. e23010. Date of Electronic Publication: 2022 Feb 21.
DOI: 10.1002/jbt.23010
Abstrakt: Background: Sodium benzoate (SB) is a widely used food preservative. However, excessive intake of a high dose of SB poses a risk of neurotoxicity. Ascorbic acid (AA) is a naturally occurring antioxidant found in fruits with reported neuroprotective properties. The present study investigated the neurobehavioral and biochemical alterations in SB-treated rats and the ameliorative effect of AA in rats.
Methods: Forty-two male Wistar rats were divided into six groups (n = 7). Group 1 (vehicle, 10 ml/kg), Groups 2-4 rats SB (150, 300, and 600 mg/kg), Group 5 AA (100 mg/kg) and Group 6 (SB 600 mg/kg + AA 100 mg/kg). Treatment was daily administered for 28 days by oral route. Anxiogenic behavior, locomotor, and exploratory activities were evaluated in the open field monitored with a camera, and memory performance in Y-maze. Brain oxidative stress, inflammatory, apoptosis, and cholinergic markers were determined. The cortico-hippocampal tissues were examined histologically.
Results: SB-treated rats showed significant anxiogenic-like behavior and impairment in locomotor, exploratory, and memory performance. This was reversed in SB (600 mg/kg)-treated rats coadministered with AA. SB-treated rats showed a decrease in antioxidant enzyme activities, increase malondialdehyde (MDA), nitrite, tumor necrosis factor-alpha, caspase-3, and acetylcholinesterase activity in the striatum, hippocampus, frontal cortex, and cerebellum. These biochemical changes were reversed in AA-treated rats. Reduced cortico-hippocampal neuronal cell count and the pyknotic index were found in SB-treated rats, which was also reversed in AA-treated rats.
Conclusion: Conclusively, sodium-benzoate-induced neurobehavioral deficits and brain biochemical changes were ameliorated by ascorbic acid probably via antioxidant, anti-inflammatory, and apoptotic mechanisms.
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Databáze: MEDLINE