Swimming impairment and acetylcholinesterase inhibition in zebrafish exposed to copper or chlorpyrifos separately, or as mixtures.

Swimming impairment and acetylcholinesterase inhibition in zebrafish exposed to copper or chlorpyrifos separately, or as mixtures.
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DOI:
10.1016/j.cbpc.2010.07.008
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发表时间:
2011-01
影响因子:
3.9
通讯作者:
Gallagher, Evan P.
Gallagher, Evan P.
中科院分区:
环境科学与生态学3区
文献类型:
--
作者:
Tilton, Fred A.;Bammler, Theo K.;Gallagher, Evan P.

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毒死蜱(CPF)等农药和铜等金属会损害鱼类的游泳行为。然而,暴露于神经毒物的混合物对游泳行为的影响很少受到关注。在目前的研究中,我们分析了自发游泳率的成年斑马鱼(Danio rerio),调查在体内混合物的相互作用,涉及两个化学类。以斑马鱼为实验动物,分别暴露于0.1 μM、0.25 μM、0.6 μM、6.3、16、40 ppb的氯化铜(CuCl)、0.1 μM、0.25 μM、0.6 μM、35、88、220 ppb的毒死蜱(CPF)及其二元混合物中24 h,以了解铜对CPF神经毒性的影响。暴露于CPF增加了经历冻结反应(一种反捕食者行为)的动物数量,并且在最高CPF剂量(0.6 μM)下,引起斑马鱼游泳率下降。有趣的是,添加铜导致CPF暴露组中经历冷冻反应的斑马鱼数量减少。没有证据表明铜和CPF之间的相加或协同毒性。虽然CPF显著降低了肌肉AChE活性,但肌肉AChE浓度与游泳行为之间的关系相对较差,表明游泳行为丧失的非肌肉AChE机制。总之,我们观察到铜对CPF游泳损伤的调节作用,似乎涉及AChE和非AChE机制。我们的研究支持斑马鱼在理解化学混合物相互作用和神经行为损伤方面的效用。
Pesticides such as chlorpyrifos (CPF) and metals such as copper can impair swimming behavior in fish. However, the impact to swimming behavior from exposure to mixtures of neurotoxicants has received little attention. In the current study, we analyzed spontaneous swimming rates of adult zebrafish (Danio rerio) to investigate in vivo mixture interactions involving two chemical classes. Zebrafish were exposed to the neurotoxicants copper chloride (CuCl, 0.1 μM, 0.25 μM, 0.6 μM, or 6.3, 16, 40 ppb), chlorpyrifos (CPF, 0.1 μM, 0.25 μM, 0.6 μM, or 35, 88, 220 ppb) and binary mixtures for 24 hr to better understand the effects of Cu on CPF neurotoxicity. Exposure to CPF increased the number of animals undergoing freeze responses (an anti-predator behavior) and, at the highest CPF dose (0.6 μM), elicited a decrease in zebrafish swimming rates. Interestingly, the addition of Cu caused a reduction in the number of zebrafish in the CPF-exposure groups undergoing freeze responses. There was no evidence of additive or synergistic toxicity between Cu and CPF. Although muscle AChE activity was significantly reduced by CPF, there was a relatively poor relationship among muscle AChE concentrations and swimming behavior, suggesting non-muscle AChE mechanisms in the loss of swimming behavior. In summary, we have observed a modulating effect of Cu on CPF swimming impairment that appears to involve both AChE and non-AChE mechanisms. Our study supports the utility of zebrafish in understanding chemical mixture interactions and neurobehavioral injury.
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