Inhibition of brain AChE in brook trout by aminocarb and its toxic metabolites.

S Y Szeto, K M Sundaram, J Feng

Index: J. Environ. Sci. Health B 20(5) , 559-75, (1985)

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Abstract

In-vitro inhibitions of brain AChE in brook trout, Salvelinus fontinalis (Mitchill), by aminocarb (4-dimethylamino-m-tolyl N-methylcarbamate) and its toxic metabolites, MAA (4-methylamino-m-tolyl N-methylcarbamate), AA(4-amino-m-tolyl N-methylcarbamate), MFA (4-methylformamido-m-tolyl N-methylcarbamate) and FA (4-formamido-m-tolyl N-methylcarbamate) were investigated. The molar concentrations of inhibitors causing 50% inhibition (I50s) were AA (3.62 X 10(-6] less than MAA (7.92 X 10(-6] less than aminocarb (1.01 X 10(-5] less than MFA (4.29 X 10(-5] less than FA (7.11 X 10(-5]. After exposure of fish to various concentrations of aminocarb (25, 250 and 2500 ppb) and MAA (25, 250, 500 and 2500 ppb) at 9 degrees C in dechlorinated tap water for 96 h, inhibitions of brain AChE ranged from 13 to 77%. Mortality occurred only in fish exposed to 500 ppb (22%) and 2500 ppb (100%) of MAA. Enzyme activities recovered to the control levels 12 to 96 h after the fish had been transferred to clean water for clearing; in survivors of the 500-ppb MAA exposure, however, AChE activities decreased again thereafter.