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Abstract: Alcohol abuse is a health problem throughout the world and alcohol consumption is linked to the occurrence of several pathological conditions. Acute ethanol administration exerts a variety of actions on the central nervous system (CNS). Zebrafish has been used as an attractive model system to investigate behavioral and neurochemical changes promoted by alcohol intoxication. Here we investigated the in vitro and in vivo effects promoted by ethanol and its metabolites on zebrafish brain acetylcholinesterase (AChE). There was a significant increase of AChE (33%) activity after acute 1% ethanol exposure. However, ethanol in vitro did not alter AChE activity. Acetaldehyde, the first metabolite of alcohol metabolism, promoted a dose-dependent decrease (15%, 27.5% and 46.5%) at 0.25%, 0.5% and 1%, respectively. Acetate, a product of acetaldehyde degradation, did not change AChE activity. Furthermore, the acute ethanol exposure was able to inhibit AChE transcripts at 0.5% and 1%. These findings suggest that the alterations on zebrafish AChE could reveal molecular mechanisms related to cholinergic signaling in alcoholism. [Copyright &y& Elsevier]

Abstract: 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. [Copyright &y& Elsevier]

Binge drinking is characterized by excessive alcohol consumption in a short period of time and is associated with a poor quality of life. Zebrafish are commonly used to investigate neurochemical, behavioral, and genetic parameters associated with ethanol (EtOH) exposure. However, few studies have used zebrafish as a model to investigate binge EtOH exposure. In order to elucidate the potential neurobehavioral impairments evoked by binge EtOH exposure in zebrafish, animals were immersed in 1.4% EtOH for 30 min three consecutive times with intervals of one week. Neurobehavioral parameters were analyzed immediately following the third exposure, as well as 2 and 9 days later. Brain choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities were reduced 9 days after the treatment. Thiobarbituric acid-reactive species and dichlorodihydrofluorescein levels were increased immediately after the treatment, but both returned to normal levels 2 days after the treatment. Catalase and glutathione reductase were impaired 2 and 9 days after the treatment. No alteration was observed in superoxide dismutase and glutathione peroxidase activities. EtOH treatment did not alter brain expression of inflammatory genes such as il - 1 β, il - 10 , and tnf -α. Zebrafish displayed anxiolytic-like behavior immediately after the last exposure, though there was no behavioral alteration observed 9 days after the treatment. Therefore, binge EtOH exposure in zebrafish leads to long lasting brain cholinergic alteration, probably related to oxidative stress immediately after the exposure, which is independent of classical inflammatory markers. • Brain AChE and ChAT activities were reduced 9 days after weekly-binge EtOH exposure in zebrafish. • Oxidative stress and antioxidant enzymes were altered after weekly-binge EtOH exposure. • Zebrafish behavior was altered 2 days, but not 9 days, after weekly-binge EtOH exposure. [ABSTRACT FROM AUTHOR]