PUBLICATION
Influence of mercury chloride on adenosine deaminase activity and gene expression in zebrafish (Danio rerio) brain
- Authors
- Senger, M.R., Rosemberg, D.B., Seibt, K.J., Dias, R.D., Bogo, M.R., and Bonan, C.D.
- ID
- ZDB-PUB-100317-29
- Date
- 2010
- Source
- Neurotoxicology 31(3): 291-296 (Journal)
- Registered Authors
- Bonan, Carla Denise
- Keywords
- adenosine, adenosine deaminase, zebrafish, brain, toxic metals, mercury
- MeSH Terms
-
- Actins/genetics
- Actins/metabolism
- Adenosine Deaminase/classification
- Adenosine Deaminase/genetics
- Adenosine Deaminase/metabolism*
- Analysis of Variance
- Animals
- Brain/drug effects*
- Brain/enzymology
- Brain/physiopathology
- Chelating Agents/pharmacology
- Disinfectants/pharmacology*
- Dithiothreitol/pharmacology
- Dose-Response Relationship, Drug
- Edetic Acid/pharmacology
- Mercuric Chloride/pharmacology*
- Zebrafish/anatomy & histology*
- PubMed
- 20226812 Full text @ Neurotoxicology
- CTD
- 20226812
Citation
Senger, M.R., Rosemberg, D.B., Seibt, K.J., Dias, R.D., Bogo, M.R., and Bonan, C.D. (2010) Influence of mercury chloride on adenosine deaminase activity and gene expression in zebrafish (Danio rerio) brain. Neurotoxicology. 31(3):291-296.
Abstract
Mercury is a widespread environmental contaminant that is neurotoxic even at very low concentrations. In this study we investigated the effects of mercury chloride on soluble and membrane adenosine deaminase (ADA) activity and gene expression in zebrafish brain. Inhibition of ADA activity was observed in the soluble fraction at 5 to 250muM HgCL(2) (84.6-92.6%, respectively), whereas inhibition occurred at 50 to 250muM in membrane fractions (20.9-26%, respectively). We performed in vitro experiments with chelants (EDTA and DTT) to test if these compounds prevented or reversed the inhibition caused by HgCl(2) and found that the inhibition was partially or fully abolished. The effect on ADA activity in soluble and membrane fractions was evaluated after acute (24h) and subchronic (96h) in vivo exposure of zebrafish to 20mug/L HgCl(2). ADA activity in the soluble fraction was decreased after both acute (24.5%) and subchronic (40.8%) exposures, whereas in brain membranes the enzyme was inhibited only after subchronic exposure (21.9%). Semiquantitative RT-PCR analysis showed that HgCl(2) did not alter ADA gene expression. This study demonstrated that ADA activity was inhibited by mercury and this effect might be related to the neurotoxicity of this heavy metal.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping