Zinc supplement reverses short-term memory deficit in sodium benzoate-induced neurotoxicity in male Wistar rats by enhancing anti-oxidative capacity via Nrf 2 up-regulation

Sodium benzoate (SB) is a commonly-used food preservative, with a controversial report to its neurological benefit and toxicity. Zinc (Zn) is a trace element that plays a crucial role in memory, inflammation and oxidative stress. This study was to investigate the effect of SB on rat cognition and me...

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Bibliographic Details
Published in:Behavioural brain research 2023-02, Vol.437, p.114163, Article 114163
Main Authors: Akintoye, O.O., Ajibare, A.J., Folawiyo, M.A., Jimoh-Abdulghaffaar, H.O., Asuku, A., Owolabi, G.A., Babalola, K.T.
Format: Article
Language:English
Subjects:
Acetylcholinesterase - metabolism
Animals
Antioxidants - metabolism
Antioxidants - pharmacology
Inflammation
Male
Memory
Memory, Short-Term
Neurotoxicity Syndromes
NF-E2-Related Factor 2 - metabolism
Oxidative Stress
Rats
Rats, Wistar
Sodium benzoate
Sodium Benzoate - pharmacology
Superoxide Dismutase - metabolism
Up-Regulation
Zinc
Zinc - metabolism
Zinc - pharmacology
Zinc Sulfate
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Summary:Sodium benzoate (SB) is a commonly-used food preservative, with a controversial report to its neurological benefit and toxicity. Zinc (Zn) is a trace element that plays a crucial role in memory, inflammation and oxidative stress. This study was to investigate the effect of SB on rat cognition and memory and the possible modulatory effect of Zn supplement. Twenty four male Wistar rats were divided into four groups of six animals each. Animals in groups 1–4 were treated with normal saline 1 ml/kg, SB 200 mg/kg, zinc sulphate 10 ml/kg and SB 200 mg/kg + zinc sulphate 10 ml/kg/day daily respectively for three weeks. After treatment, the animals were subjected to different behavioural tests, and then sacrificed. Their blood samples were collected for catalase(CAT), superoxide dismutase(SOD) and interleukin-1B(IL-1B) assay. Brain samples were also collected for nuclear factor-erythroid-related factor 2(Nrf2), and acetylcholinesterase (AchE) mRNA gene expression. The serum levels of CAT and SOD were (p 
ISSN:0166-4328
1872-7549
DOI:10.1016/j.bbr.2022.114163