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

• Published in: Journal of biochemical and molecular toxicology 2022-05, Vol.36 (5), p.e23010-n/a
• Main Authors: Asejeje, Folake O., Ajayi, Babajide O., Abiola, Michael A., Samuel, Omolola, Asejeje, Gbolahan I., Ajiboye, Ebenezer O., Ajayi, Abayomi M.
• Format: Article
• Language: English
• Subjects: Acetylcholinesterase; Antioxidants; Apoptosis; Ascorbic acid; Benzoic acid; Biochemistry; Brain; Caspase; caspase‐3; Cerebellum; Cholinergics; Cognitive ability; Cortex (frontal); Enzymatic activity; Exploratory behavior; Food intake; Hippocampus; Inflammation; Males; Neostriatum; neurobehavioral deficits; Neuroprotection; Neurotoxicity; Oral administration; Oxidative stress; Preservatives; Rodents; Sodium; Sodium benzoate
• ISSN: 1095-6670; 1099-0461
• DOI: 10.1002/jbt.23010

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.