PUBLICATION

Adenosine deaminase activity and gene expression patterns are altered after chronic ethanol exposure in zebrafish brain

Authors
Rico, E.P., Rosemberg, D.B., Berteli, J.F.A., da Silveira Langoni, A., Souto, A.A., Bogo, M.R., Bonan, C.D., Souza, D.O.
ID
ZDB-PUB-171111-7
Date
2018
Source
Neurotoxicology and teratology   65: 14-18 (Journal)
Registered Authors
Bonan, Carla Denise
Keywords
Adenosine deaminase, Chronic, Ethanol, Zebrafish
MeSH Terms
  • Adenosine Deaminase/genetics
  • Adenosine Deaminase/metabolism*
  • Animals
  • Brain/drug effects*
  • Brain/enzymology
  • Dose-Response Relationship, Drug
  • Ethanol/toxicity*
  • Female
  • Gene Expression/drug effects*
  • Male
  • Zebrafish/genetics
  • Zebrafish/metabolism*
PubMed
29122710 Full text @ Neurotoxicol. Teratol.
Abstract
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.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping