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金鱼线粒体代谢在体外暴露于 Cd、Cu 和 Ni 下的抑制作用。

Inhibition of goldfish mitochondrial metabolism by in vitro exposure to Cd, Cu and Ni.

机构信息

Institut National de la Recherche Scientifique, Centre - Eau Terre Environnement, 490 rue de la Couronne, Québec, QC, Canada G1K 9A9.

出版信息

Aquat Toxicol. 2010 Jun 10;98(2):107-12. doi: 10.1016/j.aquatox.2010.01.020. Epub 2010 Feb 6.

DOI:10.1016/j.aquatox.2010.01.020
PMID:20207426
Abstract

Although impairment of aerobic capacities has been reported in metal-contaminated wild fish, little is known about the direct toxicity of the metals themselves at the low concentrations found in the field compared to indirect consequences mediated by metal effects on ecological variables such as prey type and abundance, predation and competition. This study examined the in vitro effects of Cd, Cu and Ni on mitochondrial enzyme activity and maximal (State 3) mitochondrial oxygen consumption rate in goldfish (Carassius auratus) tissues at concentrations representative of values reported in wild metal-contaminated fish. There was little effect of adding metals to liver or muscle homogenates on the activity of citrate synthase (CS), although a slight inhibition of liver CS was observed at the highest Cd concentration tested. In contrast, adding high concentrations of Ni to muscle homogenates increased muscle CS activity. Unlike CS, the metalloenzyme cytochrome C oxidase (CCO) was quite sensitive to metal additions; its activity was consistently enhanced by all three metals tested. When added to liver mitochondrial preparations, both Cd and Cu strongly inhibited State 3 respiration. In contrast, Ni did not affect mitochondrial respiration even at the highest concentration tested. Taken together, these results demonstrate that low concentrations of Cd, Cu and Ni have toxic effects on mitochondrial metabolism and enzyme activities and suggest that the inhibition of aerobic capacities frequently reported for wild metal-contaminated fish is at least partly due to metal effects on mitochondrial function, although the mechanisms probably do not involve direct enzyme inhibition.

摘要

尽管有报道称受金属污染的野生鱼类的有氧能力受损,但与金属对生态变量(如猎物类型和丰度、捕食和竞争)的间接影响相比,在野外发现的低浓度下金属本身的直接毒性知之甚少。本研究在体外检查了 Cd、Cu 和 Ni 在金鱼(Carassius auratus)组织中的线粒体酶活性和最大(状态 3)线粒体耗氧量的影响,其浓度代表了受金属污染的野生鱼类中报告的值。尽管在测试的最高 Cd 浓度下观察到肝脏 CS 轻微抑制,但向肝或肌肉匀浆中添加金属对柠檬酸合酶(CS)的活性几乎没有影响。相比之下,向肌肉匀浆中添加高浓度的 Ni 会增加肌肉 CS 活性。与 CS 不同,金属酶细胞色素 C 氧化酶(CCO)对金属添加非常敏感;三种测试金属均一致增强了其活性。当添加到肝线粒体制剂中时,Cd 和 Cu 均强烈抑制状态 3 呼吸。相比之下,即使在测试的最高浓度下,Ni 也不会影响线粒体呼吸。综上所述,这些结果表明,低浓度的 Cd、Cu 和 Ni 对线粒体代谢和酶活性具有毒性作用,这表明经常报道的受金属污染的野生鱼类的有氧能力受损至少部分归因于金属对线粒体功能的影响,尽管其机制可能不涉及直接的酶抑制。

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