Taurine prevents enhancement of acetylcholinesterase activity induced by acute ethanol exposure and decreases the level of markers of oxidative stress in zebrafish brain.
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-aminoethanesulfonic acid) is a β-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 lipoperoxidation. 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.
Rosemberg
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DB
Programa de Pós-graduação em Bioquímica, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos 2600-Anexo, 90035-003, Porto Alegre, RS, Brazil. dbrosemberg@gmail.com
da Rocha
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RF
Rico
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Zanotto-Filho
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Dias
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RD
Bogo
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Bonan
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CD
Moreira
J C F
JC
Klamt
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Souza
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D000110:Acetylcholinesterase / Q000187:drug effects* / Q000378:metabolism; D020268:Alcohol-Induced Disorders, Nervous System / Q000188:drug therapy* / Q000201:enzymology / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D002800:Cholinesterase Inhibitors / Q000378:metabolism / Q000494:pharmacology*; D004195:Disease Models, Animal; D005260:Female; D008297:Male; D018696:Neuroprotective Agents / Q000378:metabolism / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D013045:Species Specificity; D013654:Taurine / Q000378:metabolism / Q000494:pharmacology*; D015027:Zebrafish
D002800:Cholinesterase Inhibitors; D018696:Neuroprotective Agents; D013654:Taurine; D000110:Acetylcholinesterase