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Treatment with N-acetylcysteine and/or zinc sulfate restores neurobehavioral functions through modulation of neurochemical activities in mice exposed to bonny light crude oil

Background Bonny light crude oil is a major economy-driving factor in developing countries. However, it is associated with behavioral abnormalities such as anxiety and depression. Meanwhile, it is not certain whether treatment with zinc sulfate (ZnSO 4 ) and/or N -acetyl cysteine (NAC) would reverse...

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Published in:Nutrire : revista de Sociedade Brasileira de Alimentação e Nutrição = journal of the Brazilian Society of Food and Nutrition 2024-01, Vol.49 (1), p.4, Article 4
Main Authors: Naiho, Alexander Obidike, Asiwe, Jerome Ndudi, Obore, Eruore Amalaka, Okopi, Adakole, Olatuyi, Olalekan Marvelous, Chimezie, Joseph, Nekabari, Miracle Kii
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Language:English
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Summary:Background Bonny light crude oil is a major economy-driving factor in developing countries. However, it is associated with behavioral abnormalities such as anxiety and depression. Meanwhile, it is not certain whether treatment with zinc sulfate (ZnSO 4 ) and/or N -acetyl cysteine (NAC) would reverse the neurobehavioral alterations caused by exposure to bonny light crude oil (BLCO). Therefore, we investigated the effect of ZnSO 4 and/or NAC on bonny light crude oil-induced neurobehavioral deficit. Methods Forty (40) adult male Swiss mice were randomly assigned to five groups ( n  = 8). Group 1 received standard feed, group 2 was given BLCO (2 ml/20 g of feed) for 14 days while groups 3–5 were treated with NAC (100 mg/kg), ZnSO 4 (0.5 mg/kg), and NAC + ZnSO 4 for 14 days after 14-day BLCO exposure. Locomotive, anxiolytic, and depressive-like behaviors were assessed using open-field test, elevated plus maze, light and dark box test, and force swimming test. At the end of the behavioral test, mice were sacrificed, and the brain excised for neurochemical examination. Results The protective role of ZnSO 4 and/or N -acetyl cysteine was demonstrated by improved locomotive activity, anxiolytic, and antidepressive-like behaviors. ZnSO 4 and/or N -acetyl cysteine also mitigated neurochemical dysregulation induced by BLCO as evidence in upregulating dopamine, norepinephrine, and serotonin neurotransmission and decreased glutamate, acetylcholinesterase as well as monoamine oxidase activities. Conclusion Treatment with ZnSO 4 and/or N -acetyl cysteine reverses BLCO-induced neurobehavioral alterations via modulation of neurochemical activities.
ISSN:2316-7874
1519-8928
2316-7874
DOI:10.1186/s41110-023-00249-0