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 5-250 microM HgCl(2) (84.6-92.6%, respectively), whereas inhibition occurred at 50-250 microM 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 20 microg/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.
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