• Jotele Fontana Agostini, Glaucia Dal Santo, Samira Leila Baldin, Henrique Teza Bernardo, Ana Caroline Salvador de Farias, Eduardo Pacheco Rico, and Almir Gonçalves Wanderley.
• Department of Pharmaceutical Sciences, Federal University of Pernambuco (UFPE), Recife, PE, Brazil.
• Neuroscience. 2021 Feb 10; 455: 251-262.

AbstractGallic acid (GA) is a polyphenolic compound that has attracted significant interest due to its antioxidant action through free radical elimination and metal chelation. Ethanol is a highly soluble psychoactive substance, and its toxicity is associated with oxidative stress. In this context, the purpose of the present study was to investigate the effect of GA on neurochemical changes in zebrafish brains exposed to ethanol. GA was first analyzed in isolation by treating the animals at concentrations of 5, 10, and 20 mg/L for 24 h and 48 h. The results revealed that the group exposed to 20 mg/L over a 24/48 h period exhibited increases in thiobarbituric acid reactive substance (TBA-RS) levels and 2',7'-dichlorofluorescein (DCFH) oxidation, demonstrating a pro-oxidant profile. Moreover, decrease in acetylcholinesterase (AChE) enzyme activity was observed. To investigate the effects of GA after ethanol exposure, the animals were divided into four groups: control; those exposed to 0.5% ethanol for 7 days; those exposed to 0.5% ethanol for 7 days and treated with GA at 5 and 10 mg/L on day 8. Treatment with GA at 5 and 10 mg/L reversed impairment of choline acetyltransferase activity and the damage to TBA-RS levels, DCFH oxidation, and superoxide dismutase activity induced by ethanol. Results of the present study suggest that GA treatment (20 mg/L) appeared to disrupt oxidative parameters in the zebrafish brain. GA treatment at 5 and 10 mg/L reversed alterations to the cholinergic system induced by prolonged exposure to ethanol in the zebrafish brain, probably through an antioxidant mechanism.Copyright © 2020 IBRO. Published by Elsevier Ltd. All rights reserved.

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