慢性乙醇暴露后斑马鱼大脑中的腺苷脱氨酶活性和基因表达模式发生改变。
Adenosine deaminase activity and gene expression patterns are altered after chronic ethanol exposure in zebrafish brain.
机构信息
Programa de Pós-Graduação em Ciências da Saúde, Laboratório de Sinalização Neural e Psicofarmacologia, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Av. Universitária, 1105, Bloco S, Sala 6, Bairro Universitário, Criciúma, SC, Brazil; Instituto Nacional de Ciência e Tecnologia em Excitotoxicidade e Neuroproteção (INCT-EN), 90035-003 Porto Alegre, RS, Brazil.
Programa de Pós-Graduação em Bioquímica Toxicológica, Departamento de Bioquímica e Biologia Molecular, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, RS, 97105-900 Santa Maria, RS, Brazil; Instituto Nacional de Ciência e Tecnologia em Excitotoxicidade e Neuroproteção (INCT-EN), 90035-003 Porto Alegre, RS, Brazil.
出版信息
Neurotoxicol Teratol. 2018 Jan-Feb;65:14-18. doi: 10.1016/j.ntt.2017.11.001. Epub 2017 Nov 7.
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 28days. 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 28days (44%) of ethanol exposure. ADA1 was not altered whereas mRNA transcript levels for ADAL presented an increase after 28days of ethanol exposure (34%). ADA2-1 showed a decrease (26%) followed by an increase (17%) of transcripts after 14 and 28days of ethanol exposure, respectively. However, ADA2-1 truncated alternative splice isoform (ADA2-1/T) demonstrated a reduction after 28days (20%). ADA2-2 was decreased (22%) followed by an increase (109%) of transcripts after 14 and 18days of ethanol exposure, respectively. Altogether, the purine catabolism promoted by ADA may be an important target of the chronic toxicity induced for ethanol.
乙醇改变了兴奋性和抑制性神经递质之间的平衡，其中毒会导致包括信号转导在内的多种反应发生变化。最近，斑马鱼被用于研究乙醇对行为和生化参数的长期影响。本研究旨在评估斑马鱼大脑中的腺苷酸脱氨酶（ADA）可溶性和膜结合活性及其基因表达。动物被暴露于 0.5%乙醇中 7、14 和 28 天。所有处理后，可溶性部分的 ADA 活性均无明显变化。然而，我们发现，经过 28 天的乙醇暴露后，膜部分的 ADA 活性下降了 44%。ADA1 没有改变，而 ADAL 的 mRNA 转录水平在 28 天的乙醇暴露后增加了 34%。ADA2-1 先下降（26%），然后在 14 和 28 天的乙醇暴露后分别增加（17%）。然而，ADA2-1 的截断的选择性剪接异构体（ADA2-1/T）在 28 天后减少了 20%。ADA2-2 先下降（22%），然后在 14 和 18 天的乙醇暴露后分别增加（109%）。总之，ADA 介导的嘌呤分解代谢可能是乙醇慢性毒性的一个重要靶点。
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