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Time course of inhibition and recovery following acute and subacute organophosphate and carbamate exposure in the goldfish
ANA FERRARI; VENTURINO ANDRÉS; PECHÉN DE D'ANGELO ANA M
Congreso; 27th meeting of the Federation of European Biochemical Societies (FEBS) and Pan-American Association for Biochemistry and Molecular Biology (PABMB); 2001
Toxicity data contrasting mortality and brain cholinesterase inhibition in the goldfish (Carassius auratus) are presented. Brain cholinesterase (ChE) was greatly reduced after 96 h of exposure in vivo at sub-lethal concentrations of azinphosmethyl and parathion. The inhibition of the enzyme was dose-dependent and concentrations higher than 0.1 mgáL-1 caused more than 90% of inhibition. The effect of carbaryl was less pronounced, achieving a 86% of inhibition at concentrations corresponding to the CL50. After in vivo exposure to sub-lethal concentrations of parathion and azinphosmethyl (0.1 mg/L-1) and carbaryl (3.0 mg/L-1) the activity of the goldfish brain ChE was greatly reduced. In the following 96 h of recovery, the enzyme inhibited with carbaryl was restored to 75% activity, while the enzyme inhibited with organophosphates (OPs) required more than 35 days for recovery. Goldfish were able to withstand high percentages of brain ChE inhibition without mortality suggesting that another target/s may be responsible for the lethal effects. However, the enzyme is a good biomarker of acute and subacute exposure to OPs and carbamates.