Ferrari Ana, Venturino Andres, de D'Angelo Ana M Pechen
LIBIQUIMA Department of Chemistry, Universidad Nacional del Comahue, 8300 Neuquen, Buenos Aires 1400, Argentina.
Ecotoxicol Environ Saf. 2004 Mar;57(3):420-5. doi: 10.1016/S0147-6513(02)00069-6.
Laboratory toxicity data contrasting mortality and brain cholinesterase inhibition in the goldfish (Carassius auratus) are presented. Brain cholinesterase (ChE) was greatly reduced after 96 h of exposure in vivo at sublethal concentrations of azinphosmethyl and parathion. The inhibition of the enzyme was dose dependent, and concentrations higher than 0.1mg/L caused more than 90% inhibition. The effect of carbaryl was less pronounced, achieving an 86% inhibition at concentrations corresponding to the 96-h LC50. After in vivo exposure to sublethal concentrations of parathion and azinphosmethyl (0.1 mg/L) and carbaryl (3.0 mg/L), the activity of the goldfish brain ChE was greatly reduced. In the following 96 h of recovery, the enzyme inhibited with carbaryl was restored to 75% activity, while the enzyme inhibited with organophosphates (OPs) required more than 35 days for recovery. Goldfish were able to withstand high percentages of brain ChE inhibition without mortality, suggesting that another target may be responsible for the lethal effects. However, the enzyme is a good biomarker of acute and subacute exposure to OPs and carbamates.
本文给出了对比金鱼（Carassius auratus）死亡率和脑胆碱酯酶抑制作用的实验室毒性数据。在体内以亚致死浓度暴露于谷硫磷和对硫磷96小时后，脑胆碱酯酶（ChE）大幅降低。该酶的抑制作用呈剂量依赖性，浓度高于0.1mg/L时会导致超过90%的抑制率。西维因的作用不太明显，在相当于96小时半数致死浓度（LC50）的浓度下，抑制率达到86%。在体内暴露于亚致死浓度的对硫磷、谷硫磷（0.1mg/L）和西维因（3.0mg/L）后，金鱼脑ChE的活性大幅降低。在随后96小时的恢复过程中，被西维因抑制的酶恢复到75%的活性，而被有机磷（OPs）抑制的酶恢复活性则需要超过35天。金鱼能够承受高比例的脑ChE抑制而不死亡，这表明可能另有靶点导致致死效应。然而，该酶是急性和亚急性暴露于有机磷和氨基甲酸酯类的良好生物标志物。
