Lethal and sublethal effects of fenitrothion, an organophosphate insecticide, were investigated in rainbow trout (Salmo gairdneri) embryos, sac fry, fingerlings, and adults. Embryos first exhibited cholinesterase activity 14 days before hatch. Embryos and sac fry at various ages subjected to 34 mg/litre fenitrothion for 24 h under static exposure conditions first exhibited mortality 6 days after hatch. A 24-h lethal concentration of 50 percent of organisms (LC50) of 3.4 mg/litre and a 96-h LC50 of 2.0 mg/litre were obtained using fingerlings exposed to fenitrothion in a flow-through system. Fingerlings surviving 96 h of exposure exhibited cholinesterase activities ranging from 13 to 25 percent of controls (brain) and 30 to 51 percent (skeletal muscle). Adult trout were monitored for electrocardiogram and respiratory responses to fenitrothion concentrations of 5.0, 1.0, and 0.5 mg/litre. At 5 mg/litre, heart rate decreased initially but recovered within 24 h. Cough frequency was directly related to fenitrothion concentration. Based on acute mortality tests, the embryological life stage was the least sensitive, the sac fry stage was intermediate, and the life stages of fingerlings and adults were the most sensitive. The sublethal responses, cholinesterase inhibition in fingerlings and the cough response in adult trout, were sensitive to 0.75 and 0.5 mg/litre fenitrothion.
The detection of organophosphate (OP) insecticide pollution in natural waters requires knowledge of the physiological target sites and the mechanism of action of these chemicals in fish. This study was designed to determine the acute lethality of acephate (ATE), a phosphoramidothioate, and fenitrothion (FTN), a phosphorothionate, on rainbow trout fingerlings at three test temperatures; the sublethal effects of ATE and FTN on heart rate (HR), ventilation rate (VR), buccal amplitude (BA), and cough frequency (CF) in adult rainbow trout; and the effects of ATE and FTN on the brain, erythrocyte, gill, heart, serum, and skeletal muscle cholinesterase inhibition (ChEI) in these fish. From our results, the LC50 values of ATE were approximately 600 to 1000 times greater than those of FTN. Temperature affected the LC50 values, median survival times, and slopes of mortality curves of FTN, but not those of ATE. Both insecticides produced a decrease in HR, and an increase in VR and BA. FTN produced an increase in CF, but ATE did not. The cholinesterase activity in the erythrocytes, gill, heart, and serum showed marked inhibition after 3 h of exposure to ATE, compared with 1 h of exposure to FTN. More time was required to attain maximal inhibition in the brain and skeletal muscle than in other tissues. This study indicates that the cardiovascular and respiratory systems in fish are important sites of action for OP toxicity, and that this toxicity depends on physicochemical properties, for example, lipid solubility, and on environmental factors, for example, temperature.
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