期刊
NEUROSCIENCE
卷 171, 期 3, 页码 683-692出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2010.09.030
关键词
taurine; ethanol; acetylcholinesterase; oxidative stress parameters; zebrafish; brain
资金
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
- INCT para Excitotoxicidade e Neuroprotecao
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
- Fundacao de Amparo a Pesquisa do Estado do Rio Grande do Sul (FAPERGS)
- FINEP [01.06.0842-00]
Ethanol (EtOH) is a drug widely consumed throughout the world that promotes several neurochemical disorders. Its deleterious effects are generally associated with modifications in oxidative stress parameters, signaling transduction pathways, and neurotransmitter systems, leading to distinct behavioral changes. Taurine (2-aminoethane-sulfonic acid) is a beta-amino acid not incorporated into proteins found in mM range in the central nervous system (CNS). The actions of taurine as an inhibitory neurotransmitter, neuromodulator, and antioxidant make it attractive for studying a potential protective role against EtOH-mediated neurotoxicity. In this study, we investigated whether acute taurine cotreatment or pretreatment (1 h) prevent EtOH-induced changes in acetylcholinesterase (AChE) activity and in oxidative stress parameters in zebrafish brain. The results showed that EtOH exposure (1% in volume) during 1 h increased AChE activity, whereas the cotreatment with 400 mg.L-1 taurine prevented this enhancement. A similar protective effect of 150 and 400 mg.L-1 taurine was also observed when the animals were pretreated with this amino acid. Taurine treatments also prevented the alterations promoted in superoxide dismutase and catalase activities by EtOH, suggesting a modulatory role in enzymatic antioxidant defenses. The pretreatment with 150 and 400 mg.L-1 taurine significantly increased the sulfydryl levels as compared to control and EtOH groups. Moreover, 150 and 400 mg.L-1 taurine significantly decreased thiobarbituric acid reactive species (TBARS) levels, but the cotreatment with EtOH plus 400 mg.L-1 taurine did not prevent the EtOH-induced lipoper-oxidation. In contrast, the pretreatment with 150 and 400 mg.L-1 taurine prevented the TBARS increase besides decreased the basal levels of lipid peroxides. Altogether, our data showed for the first time that EtOH induced oxidative stress in adult zebrafish brain and reinforce the idea that this vertebrate is an attractive alternative model to evaluate the beneficial effect of taurine against acute EtOH exposure. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据