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The effect of a long-term exposure of tenchs to different concentrations (10 and 100 micro g/L) of the pesticide carbofuran has been evaluated. Microsomal hepatic cytochrome P450 subfamily 1A (CYP1A) and 3A (CYP3A) activities, as well as the phase II enzyme uridine diphospho-glucuronosyltransferase (UDPGT) activity were evaluated as adequate biomarkers of fish exposure to environmentally relevant concentrations of the pesticide carbofuran in freshwater ecosystems. A clear time-dependent inhibition of both CYP1A and UDPGT activities was observed in fish exposed to the highest dose of carbofuran with respect to controls, whereas in the case of CYP3A activity, values of exposed animals did not show a clear pattern of alteration during the experiment. The results of the present study demonstrated that hepatic CYP1A and UDPGT activities from tench could be considered as sensitive biomarkers for carbamate pesticides in polluted water, thus allowing future and ecologically relevant biomonitoring studies with this species.

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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.