Abstract-Chlorpyriphos (13 mg/kg) was administered to quail (Coturnix coturnix), and the responses of brain acetylcholinesterase (AChE) and plasma cholinesterase (ChE) were studied. Both enzymes responded rapidly, and the maximal inhibition (76.6 and 86.1%, respectively) ocurred 8 h postadministration. Plasma ChE recovered rapidly, and even on day 4, ChE values of quail that had received chlorpyriphos were higher than those of controls. The recovery of brain AChE activity was slower than that of plasma; it reached 59% of controls 2 d after chlorpyriphos administration, then it recovered slowly, and only at day 11 was its level not depressed with respect to controls. This recovery followed the logarithmic pattern Y ϭ a ϩ b(log X), where Y is the AChE activity expressed as the percentage with respect to controls and X is the day after dosing, giving a significant correlation (r ϭ 0.9746, p Ͻ 0.001 when using group means and r ϭ 0.9219, p Ͻ 0.001 when using individual values). No clinical signs or mortality were observed, and histopathological observations in the central nervous system (encephalytic reaction, necrotic Purkinje cells), liver (congestion, vacuolation), and kidney (congestion, nephrosis) were not severe and did not endanger the life of the quail. Sixteen hours after chlorpyriphos administration, some quail were treated with pralidoxime, which significantly reactivated brain AChE but not plasma ChE. However, this effect did not last for the rest of the experiment; because no signs of toxicosis appeared, the experiment was not repeated.
Chlorpyriphos (13 mg/kg) was administered to quail (Coturnix coturnix), and the responses of brain acetylcholinesterase (AChE) and plasma cholinesterase (ChE) were studied. Both enzymes responded rapidly, and the maximal inhibition (76.6 and 86.1%, respectively) ocurred 8 h postadministration. Plasma ChE recovered rapidly, and even on day 4, ChE values of quail that had received chlorpyriphos were higher than those of controls. The recovery of brain AChE activity was slower than that of plasma; it reached 59% of controls 2 d after chlorpyriphos administration, then it recovered slowly, and only at day 11 was its level not depressed with respect to controls. This recovery followed the logarithmic pattern Y = a + b(log X), where Y is the AChE activity expressed as the percentage with respect to controls and X is the day after dosing, giving a significant correlation (r = 0.9746, p < 0.001 when using group means and r = 0.9219, p < 0.001 when using individual values). No clinical signs or mortality were observed, and histopathological observations in the central nervous system (encephalytic reaction, necrotic Purkinje cells), liver (congestion, vacuolation), and kidney (congestion, nephrosis) were not severe and did not endanger the life of the quail. Sixteen hours after chlorpyriphos administration, some quail were treated with pralidoxime, which significantly reactivated brain AChE but not plasma ChE. However, this effect did not last for the rest of the experiment; because no signs of toxicosis appeared, the experiment was not repeated.
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