1972•Transactions of the American Fisheries SocietyRequires access

Organophosphate Pesticides: Specific Level of Brain AChE Inhibition Related to Death in Sheepshead Minnows

David L. Coppage

Open publisher page 97 citations

Abstract

Inhibition of brain acetylcholinesterase (AChE) in sheepshead minnows, Cyprinodon variegatus, by static exposures to acute doses of Guthion, phorate, and parathion that killed 40 to 60% of the fish in 2, 24, 48, and 72 hours indicates that effect is a function of pesticide concentration and length of exposure. Inhibition to less than 87% of normal activity is necessary to indicate exposure. The greatest inhibition caused by sublethal exposures is not as great as that caused by lethal exposures. Death occurs when AChE activity falls below 17.7% of normal, and levels below this value indicate impending death from exposure even when pesticide concentration and exposure times are unknown. In single tests, phosphamidon, Cygon, malathion, EPN, Dursban, DDVP, Diazinon, Dibrom, and methyl parathion caused inbibition to less than 17.7% of normal activity when 40 to 60% of the fish were killed. These data indicate that brain AChE levels, when properly assayed, are dependable indicators of exposure and death.

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Inhibition of brain acetylcholinesterase (AChE) in sheepshead minnows, Cyprinodon variegatus, by static exposures to acute doses of Guthion, phorate, and parathion that killed 40 to 60% of the fish in 2, 24, 48, and 72 hours indicates that effect is a function of pesticide concentration and length of exposure. Inhibition to less than 87% of normal activity is necessary to indicate exposure. The greatest inhibition caused by sublethal exposures is not as great as that caused by lethal exposures. Death occurs when AChE activity falls below 17.7% of normal, and levels below this value indicate impending death from exposure even when pesticide concentration and exposure times are unknown. In single tests, phosphamidon, Cygon, malathion, EPN, Dursban, DDVP, Diazinon, Dibrom, and methyl parathion caused inbibition to less than 17.7% of normal activity when 40 to 60% of the fish were killed. These data indicate that brain AChE levels, when properly assayed, are dependable indicators of exposure and death.

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Available abstract

Inhibition of brain acetylcholinesterase (AChE) in sheepshead minnows, Cyprinodon variegatus, by static exposures to acute doses of Guthion, phorate, and parathion that killed 40 to 60% of the fish in 2, 24, 48, and 72 hours indicates that effect is a function of pesticide concentration and length of exposure. Inhibition to less than 87% of normal activity is necessary to indicate exposure. The greatest inhibition caused by sublethal exposures is not as great as that caused by lethal exposures. Death occurs when AChE activity falls below 17.7% of normal, and levels below this value indicate impending death from exposure even when pesticide concentration and exposure times are unknown. In single tests, phosphamidon, Cygon, malathion, EPN, Dursban, DDVP, Diazinon, Dibrom, and methyl parathion caused inbibition to less than 17.7% of normal activity when 40 to 60% of the fish were killed. These data indicate that brain AChE levels, when properly assayed, are dependable indicators of exposure and death.

Key concepts: Organophosphate, Aché, Pesticide, Toxicology, Acetylcholinesterase, Pharmacology, Biology, Chemistry

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