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Ethanol alters the homeostasis between excitatory and inhibitory neurotransmitters and its intoxication reveals adenosine as responsible to modify several responses including signal transduction. Zebrafish has been recently investigated for knowledge the prolonged effect of ethanol on behavioral and biochemical parameters. The aim of this study was to evaluate the soluble and membrane adenosine deaminase activities and gene expression in zebrafish brain. Animals were exposed to 0.5% ethanol for 7, 14, and 28 days. There were no significant changes in ADA activity from soluble fraction after all treatments. However, we verified a decrease of ADA activity in membrane fraction after 28 days (44%) of ethanol exposure. ADA1 was not altered whereas mRNA transcript levels for ADAL presented an increase after 28 days of ethanol exposure (34%). ADA2-1 showed a decrease (26%) followed by an increase (17%) of transcripts after 14 and 28 days of ethanol exposure, respectively. However, ADA2-1 truncated alternative splice isoform (ADA2-1/T) demonstrated a reduction after 28 days (20%). ADA2-2 was decreased (22%) followed by an increase (109%) of transcripts after 14 and 18 days of ethanol exposure, respectively. Altogether, the purine catabolism promoted by ADA may be an important target of the chronic toxicity induced for ethanol. [ABSTRACT FROM AUTHOR]

Ethanol co-laminar flow fuel cells operating at room temperature have rarely been reported, primarily due to problems associated with the kinetics of ethanol oxidation. In this work, we present a study of the effect of ethanol concentration, pH of anodic and cathodic streams, and nature of the oxidant on the performances of an acrylic cell and a paper-based, membraneless co-laminar flow fuel cell (LFFC), with total cell volumes of 14.29 cm 3 and 0.62 cm 3 , respectively. Additionally, this work reports the synthesis of a Pd-NiO anodic nanocatalyst by a simple, fast, and environmentally friendly method in order to match the clean, easy-to-use, and simple fabrication methods of these ethanol co-laminar flow fuel cells. The synthesized Pd-NiO exhibited a crystallite size of 8.1 nm and an average particle size of 8.7 nm for Pd-NiO/C. The highest performances were obtained by combining an alkaline anodic stream with an acidic cathodic stream, increasing the cell voltage, and decreasing cathodic limitations caused by the simultaneous occurrence of oxygen reduction as well as hydrogen reduction reactions. With these improvements, power densities of 108 and 85.5 mW cm −2 were obtained for the acrylic and the paper-based co-laminar flow fuel cell, respectively, which are the highest values reported to date for ethanol LFFCs at room temperature. [ABSTRACT FROM AUTHOR]

Ethanol is a widely consumed drug that acts on the central nervous system (CNS), modifying several signal transduction pathways activated by hormones and neurotransmitters. The zebrafish is an experimental model for the study of human diseases and the use of this species in biochemical and behavioral studies on alcoholism and alcohol-dependence has increased recently. However, there are no data concerning the effects of chronic ethanol exposure on the purinergic system, where extracellular nucleotides act as signaling molecules. Purinergic signaling is controlled by a group of enzymes named ectonucleotidases, which include NTPDases and ecto-5′-nucleotidase already characterized in zebrafish brain. The aim of this study was to evaluate nucleotide hydrolysis by NTPDases and ecto-5′-nucleotidase after long-term ethanol exposure. Additionally, the gene expression patterns of NTPDases1–3 and 5′-nucleotidase were determined. Animals were exposed to 0.5% ethanol for 7, 14, and 28 days. There were no significant changes in ATP and GTP hydrolysis after all treatments. However, a decrease in ADP (46% and 34%) and GDP (48% and 36%) hydrolysis was verified after 7 and 14 days, respectively. After 7 and 14 days of ethanol exposure, a significant decrease in AMP hydrolysis (48% and 36%) was also observed, whereas GMP hydrolysis was inhibited only after 7 days (46%). NTPDase2_mv and NTPDase3 mRNA transcript levels decreased after 7 and 14 days, respectively. In contrast, ethanol increased NTPDase1, NTPDase2_mq, and NTPDase3 transcript levels after 28 days of exposure. NTPDase2_mg and 5′-nucleotidase gene expression was not altered. Therefore, the ectonucleotidase pathway may be a target of chronic ethanol toxicity and the regulation of purinergic system could play a key role in the neurochemical mechanisms underlying the effects of ethanol on the CNS. [ABSTRACT FROM AUTHOR]

Abstract: This article aims to investigate the introduction, sustenance and consolidation of bioethanol in Brazil. It presents an analysis of its introductory stage, from the first decades of the 20th century until the early 1970s, when, in a second stage, additional measures allowed for its consolidation and maturity, under the widely known Proalcool. The paper presents a historical reinterpretation of the policies, mechanisms and instruments adopted in both stages, aiming to highlight the economical and political links. It is concluded that the interests of the agrarian elites, operating at the political level, and the fuel supply crisis during Second World War were basic during the first stage, to sustain a productive and logistic capacity and maintain ethanol alive as an automotive fuel. It is also concluded that the launching of Proalcool represented a transition combining the interests of the sugarcane agribusiness, burdened by the drop in sugar prices, and the need to equilibrate the balance of payments due to the oil shocks of the 1970s. Ethanol supply shocks harmed its credibility and its commercial consolidation was only possible through the introduction of flex-fuel vehicles with expectations strongly relying on climate change mitigation actions. [Copyright &y& Elsevier]

Abstract: Alcohol abuse is an acute health problem throughout the world and alcohol consumption is linked to the occurrence of several pathological conditions. Here we tested the acute effects of ethanol on NTPDases (nucleoside triphosphate diphosphohydrolases) and 5′-nucleotidase in zebrafish (Danio rerio) brain membranes. The results have shown a decrease on ATP (36.3 and 18.4%) and ADP (30 and 20%) hydrolysis after 0.5 and 1% (v/v) ethanol exposure during 60min, respectively. In contrast, no changes on 5′-nucleotidase activity were observed in zebrafish brain membranes. Ethanol in vitro did not alter ATP and ADP hydrolysis, but AMP hydrolysis was inhibited at 0.5, and 1% (23 and 28%, respectively). Acetaldehyde in vitro, in the range 0.5–1%, inhibited ATP (40–85%) and ADP (28–65%) hydrolysis, whereas AMP hydrolysis was reduced (52, 58 and 64%) at 0.25, 0.5 and 1%, respectively. Acetate in vitro did not alter these enzyme activities. Semi-quantitative expression analysis of NTPDase and 5′-nucleotidase were performed. Ethanol treatment reduced NTPDase1 and three isoforms of NTPDase2 mRNA levels. These findings demonstrate that acute ethanol intoxication may influence the enzyme pathway involved in the degradation of ATP to adenosine, which could affect the responses mediated by adenine nucleotides and nucleosides in zebrafish central nervous system. [Copyright &y& Elsevier]

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]

Baccharis trimera (Less.) DC known as "carqueja" in Brazil has been acknowledged as a medicinal plant in folk medicine for the treatment of stomach aches and gastrointestinal disorders. The present study aimed to evaluate the gastroprotective and healing effects of essential oil from B. trimera (EOBT) against gastric ulcer lesions caused by absolute ethanol and acetic acid, respectively, and to identify the mechanism of action of this essential oil in male Wistar rats. The plant material used to obtain EOBT was collected in the southern region of Brazil and was analyzed by chromatography-mass spectrometry (GCMS) demonstrate its characteristic chemical composition, with carquejyl acetate as its main component. Different doses of EOBT (50, 100, and 200 mg/kg) were administered orally in male Wistar rats as an acute treatment against absolute ethanol-induced gastric lesions. The gastric healing effect of EOBT (100 mg/kg) was evaluated once a day after 7, 10, and 14 days of treatment. After treatment, the stomachs of rats from all groups were collected to measure the lesion area (mm2), the activity of myeloperoxidase (MPO), and the relative expression of caspases −3, −8, −9, cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), vascular endothelial growth factor (VEGF), and epidermal growth factor (EGF). The zymography method was used to elucidate the activity of matrix metalloproteinase-2 (MMP-2) and −9 (MMP-9) in the healing action of EOBT. We also analyzed toxicological parameters (body weight evolution and biochemical parameters) that could result after treatment with this essential oil for 14 days. Pretreatment with EOBT (100 and 200 mg/kg) significantly decreased the severity of gastric damage induced by absolute ethanol and decreased MPO activity in gastric tissue. After 10 and 14 days of treatment with EOBT (100 mg/kg) once a day, the lesion area was significantly reduced by 61% and 65.5%, respectively, compared to the negative control group. The gastric healing effect of EOBT was followed by a decrease in the expression of COX-1 compared to that in the negative control group. Notably, treatment with EOBT for 14 days increased the expression of VEGF compared to that using an anti-ulcer drug (lansoprazole). Additionally, analyses of MMP-2 and MMP-9 activities in the gastric mucosa confirmed the accelerated gastric healing effect of EOBT, with a significant decrease in the activity of pro-MMP-2. No sign of toxicity was observed after treatment with EOBT for 14 consecutive days. Conclusion : These findings indicated that EOBT was effective in preventing and accelerating ulcer healing by decreasing MPO activity, increasing VEGF expression, and decreasing MMP-2 activity. These actions collectively contribute to the rapid recovery of gastric mucosa following treatment with EOBT, without any observed toxicity. Image 1 [ABSTRACT FROM AUTHOR]

Highlights: [•] EtOH and ALD alter glutamate uptake in zebrafish brain structures. [•] The actions of EtOH and its metabolite are concentration and structure-dependent. [•] ALD induces more severe changes on neurochemical functions in zebrafish brain. [•] Neurotoxic effects of alcohol result in changes on MTT and LDH released. [Copyright &y& Elsevier]

Taurine (TAU) is an amino sulfonic acid that plays protective roles against neurochemical impairments induced by ethanol (EtOH). Mounting evidence shows the applicability of zebrafish for evaluating locomotor parameters and anxiety-like behavioral phenotypes after EtOH exposure in a large scale manner. In this study, we assess the effects of TAU pretreatment on the behavior of zebrafish in the open tank after acute 1% EtOH (v/v) exposure (20 and 60 min of duration) and on brain alcohol contents. The exposure for 20 min exerted significant anxiolytic effects, which were prevented by 42, 150, and 400 mg/L TAU. Conversely, the 60-min condition induced depressant/sedative effects, in which the changes on vertical activity were associated to modifications on the exploratory profile. Although all TAU concentrations kept locomotor parameters at basal levels, 150 mg/L TAU, did not prevent the impairment on vertical activity of EtOH[60]. Despite the higher brain EtOH content detected in the 60-min exposure, 42, 150, and 400 mg/L TAU attenuated the increase of alcohol content in EtOH[60] group. In conclusion, our data suggest that both protocols of acute EtOH exposure induce significant changes in the spatio-temporal behavior of zebrafish and that TAU may exert a preventive role by antagonizing the effects induced by EtOH possibly due to its neuromodulatory role and also by decreasing brain EtOH levels. The hormetic dose-response of TAU on vertical exploration suggests a complex interaction between TAU and EtOH in the central nervous system. [ABSTRACT FROM AUTHOR]

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]

• Gallic acid positively modulates cholinergic damage caused by exposure to ethanol. • Gallic acid in isolation increases antioxidant activity in the zebrafish brain. • Oxidative stress induced by ethanol is regulated positively by gallic acid. Gallic 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. [ABSTRACT FROM AUTHOR]

Beer is a beverage that has been consumed worldwide for thousands of years due to social, religious, and cultural reasons; it contains polyphenolic compounds as well as phenolic acids with a potential positive effect on human health. This study aimed to explore the impact of moderate beer consumption on human health and gut microbiota diversity. Three hundred fifty-five mL of non-alcoholic beer (NAB) or alcoholic beer (AB) were consumed daily by the participants for 30 days in each study. Anthropometric measures, blood samples for biochemistry, and fecal samples for microbiota analysis were collected on Day 1 and Day 30. Microbial diversity was characterized by high-throughput sequencing of 16S rDNA libraries, and data were analyzed using the QIIME pipeline. We found that NAB and AB have effects on the composition of the gut microbiota, favoring the proliferation of Bacteroidetes with respect to Firmicutes. No increase in weight, waist, and hip parameters was observed, and the liver and lipid profile values were not modified for NAB. In addition, the consumption of NAB induced a decrease in fasting blood serum glucose and an increase in functional β cells, while, on the other hand, there was an increase in blood serum glucose and a decrease in functional β cells with the consumption of AB. In general, beer consumption neither changed anthropometric values, nor affected liver function. Although the glucose values decreased with NAB or increased with AB, they remained within the normal range. Our conclusion is that moderate consumption of NAB has a positive effect on human health via supplementation of biological active polyphenol and phenolic acids, and by enrichment of the gut microbiota diversity with beneficial bacteria, while the presence of alcohol in AB interferes with this effect. More work should be done on this topic before general conclusions are drawn. [ABSTRACT FROM AUTHOR]

Graphical abstract Abstract Quartz crystal microbalance with dissipation (QCM-D) response data was used to determine the friction coefficient (μ) between soft solid surface and ethanol. A self-assembly of Dodecanethiol (DCT) film on gold was carried out. The number of DCT grafted (Γ) onto gold surface was investigated at concentrated solutions (10–33% v/v). Such large concentration leads to an increase on grafting density, viscosity, roughness and water contact angle favoring the reduction of friction coefficient (∼0.0922). These results allow proposing a soft self-assembled hydrophobic film to reduce friction between fluids into conduit, tube, or some other device. [ABSTRACT FROM AUTHOR]

Background: Efforts aimed at reducing alcohol-related harm include early detection of risky drinkers as well as detection of early relapse in patients with alcohol dependence. Ethyl glucuronide (EtG) has been proven to be a reliable biomarker for the detection of recent drinking; however, no randomized, diagnostic trial to date has tested its impact on drinking outcomes. The aim of this study was to assess, in a randomized design, the implications of EtG screening on alcohol outcomes, compared to screening with a low sensitivity biomarker such as ethanol.Methods: Alcohol dependent outpatients were randomized to either 24 weeks of continuous screening with EtG or ethanol. Patients were aware of screening methods and results. After 24 weeks, all participants were screened with EtG. Self-reports were also gathered. A logistic regression compared the rate of EtG positive results at study end between groups. Generalized estimating equations evaluated the descending monthly rate of EtG positive patients in the EtG group.Results: A total of 162 patients were randomized. During the study period, the ethanol group showed less patients with positive screens (19/64 (29.7%) vs 58/98 (59%)). After 24 weeks, the EtG group showed a greater number of patients having a negative screening test compared to ethanol subjects when they were all screened with EtG (5/62 (8.1%) vs 13/39 (33.3%)). A significant decrease in the rate of EtG positive patients was found for the first three months of the study.Conclusions: Routine screening with EtG seems to reduce drinking and improve abstinence rates in alcohol dependent outpatients. [ABSTRACT FROM AUTHOR]

Ethanol is a widely consumed substance throughout the world. During development it can substantially damage the human fetus, whereas the developing brain is particularly vulnerable. The brain damage induced by prenatal alcohol exposure may lead to a variety of long-lasting behavioral and neurochemical problems. However, there are no data concerning the effects of developmental ethanol exposure on the glutamatergic system, where extracellular glutamate acts as signaling molecule. Here we investigated the effect of ethanol exposure for 2 h (concentrations of 0.0%, 0.1%, 0.25%, 0.50%, and 1.00%) in embryos at 24 h post-fertilization (hpf) by measuring the functionality of glutamate transporters in the brain of adult (4 months) zebrafish. However, ethanol 0.1%, 0.25% and 0.50% decreased transport of glutamate to 81.96%, 60.65% and 45.91% respectively, when compared with the control group. Interestingly, 1.00% was able to inhibit the transport activity to 68.85%. In response to the embryonic alcohol exposure, we found impairment in the function of cerebral glutamate transport in adult fish, contributing to long-term alteration in the homeostasis glutamatergic signaling. [ABSTRACT FROM AUTHOR]

Prosthesis loosening is a major problem associated with the use of poly(methyl methacrylate) (PMMA) bone cement that may be related to a peri-implant vacuolisation commonly observed at bone–cement interface. Methyl methacrylate (MMA) monomer may be one of the cement components partly responsible for the mentioned vacuolisation due to a cytotoxic effect associated to this compound. Alcoholism has been related to bone necrosis in predisposed individuals. Furthermore, ethanol has been shown to clean material with adherent cement debris during cleaning procedure in laboratory. Consequently, we have decided to study whether ethanol will also be related to an increased liberation of MMA from the polymer matrix. ‘In vitro’ release studies using PMMA plates were conducted to access the role of ethanol on the liberation of the monomer. Contact angle measurements and surface tension estimation were also carried out in order to find a possible effect of ethanol on surface cement properties. Results suggest that ethanol, even in small quantities, enhances the leaching of the monomer from the polymer matrix, but does not considerably change the wettability properties of the cement surface. [Copyright &y& Elsevier]

Background: In this study, an alternative and complementary method to those approaches currently used to estimate alcohol consumption by the population is described. This method, known as wastewater-based epidemiology (WBE), allows back-calculating the alcohol consumption rate in a given population from the concentrations of a selected biomarker measured in wastewater.Methods: Composite (24-h) wastewater samples were collected at the inlet of 17 wastewater treatment plants located in 13 Spanish cities for seven consecutive days in 2018. The sampled area covered 12.8% of the Spanish population. Wastewater samples were analyzed to determine the concentration of ethyl sulfate, the biomarker used to back-calculate alcohol consumption.Results: Alcohol consumption ranged from 4.5 to 46 mL/day/inhabitant. Differences in consumption were statistically significant among the investigated cities and between weekdays and weekends. WBE-derived estimates of alcohol consumption were comparable to those reported by its corresponding region in the Spanish National Health Survey in most cases. At the national level, comparable results were obtained between the WBE-derived annual consumption rate (5.7 ± 1.2 L ethanol per capita (aged 15+)) and that reported by the National Health Survey (4.7 L ethanol per capita (aged 15+)).Conclusions: This is the largest WBE study carried out to date in Spain to estimate alcohol consumption rates. It confirms that this approach is useful for establishing spatial and temporal patterns of alcohol consumption, which could contribute to the development of health care management plans and policies. Contrary to established methods, it allows obtaining information in a fast and relatively economical way. [ABSTRACT FROM AUTHOR]

• Ethanol withdrawal increases anxiety in zebrafish. • Ethanol withdrawal increases nitrite in zebrafish brain. • Aminoguanidine blocks both effects. • NOS-2 participates in the neurobehavioral mechanism of withdrawal. Nitric oxide has been implicated in symptoms of ethanol withdrawal in animal models. Zebrafish have been used as models to study neurobehavioral effects of ethanol (EtOH) withdrawal, but the mechanisms associated with these effects are not yet clear. Adult zebrafish were treated with 1% EtOH for 20 min per day for 8 days, injected with the nitric oxide synthase 2 (NOS-2) inhibitor aminoguanidine (50 mg/kg), and allowed to experience withdrawal (WD) in their hometanks for 7 days. EtOH WD increased anxiety-like behavior in the novel tank test, an effect that was blocked by aminoguanidine. EtOH WD also increased brain levels of nitrite, an effect that was partially blocked by aminoguanidine. These results underline a novel mechanism by which NOS-2 controls anxiety-like responses to ethanol withdrawal, with implications for the mechanistic study of symptoms associated with chronic ethanol abuse. Preprint: https://dx.doi.org/10.20944/preprints201912.0219.v1 Data and scripts: https://github.com/lanec-unifesspa/etoh-withdrawal/tree/master/NOS2 [ABSTRACT FROM AUTHOR]

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]

Binge drinking is defined as the infrequent consumption of excessive doses of alcohol in a short period of time. Zebrafish is a reliable model to investigate ethanol consumption impact on the CNS, including reward signaling like dopaminergic neurotransmission system. The aim of this study was to evaluate zebrafish brain dopaminergic parameters after intermittent weekly ethanol exposure (WEE), which mimics binge drinking. Thus, adult zebrafish were exposed to ethanol (1.4% v /v) for 30 min, once a week for three consecutive weeks. The groups were divided according to different time points after the third exposure and name as follow: immediately (WEE I), two days (WEE-2), and nine days (WEE-9) after last exposure to ethanol. Brain dopaminergic function was assessed by the activity of the dopamine transporters (DAT); monoamine oxidase (MAO) activity; dopamine and noradrenaline levels by chromatography. The WEE-I and WEE-2 groups presented a significant increase in DAT activity. The MAO activity was decreased for WEE-2 and WEE-9 groups. The WEE-2 and WEE-9 groups presented an increase in brain dopamine levels, while noradrenaline levels were not affected. Therefore, dopaminergic parameters are still altered two and nine days after the last ethanol exposure in this binge experimental model, resulting in a modulatory event in this neurotransmission pathway. Unlabelled Image • This study investigated the effects of weekly ethanol exposure in a zebrafish model. • Dopamine levels were increase 2 and 9-days after weekly-binge ethanol exposure. • Brain MAO activity was decreased after weekly-binge ethanol exposure. [ABSTRACT FROM AUTHOR]