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铜诱导三刺鱼的氧化应激:与肝金属水平的关系。

Copper-induced oxidative stress in three-spined stickleback: relationship with hepatic metal levels.

机构信息

Unité d'évaluation des risques écotoxicologiques, Direction des risques chroniques, Institut National de l'Environnement Industriel et des Risques (INERIS), BP 2, F-60550 Verneuil en Halatte, France.

出版信息

Environ Toxicol Pharmacol. 2005 Jan;19(1):177-83. doi: 10.1016/j.etap.2004.07.003.

DOI:10.1016/j.etap.2004.07.003
PMID:21783474
Abstract

The aim of this study was to characterise biomarker responses in three-spined sticklebacks exposed to copper. For this purpose, adult sticklebacks were exposed for 3 weeks to copper sulphate at 0, 25, 100 and 200μgL(-1) as Cu. At days 4, 8, 12 and 21, several parameters were measured including liver, gonad and spleen somatic indexes, hepatic biomarkers (catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione (GSH), glutathione-S-transferase (GST) and 7-ethoxyresorufin-O-deethylase (EROD)) and hepatic copper and zinc concentrations. Copper induced a rapid and transient increase of antioxidant enzymes and a depletion of glutathione content during the first 8 days of exposure. Significant copper and zinc accumulation in fish liver were observed for the two higher exposure concentrations after 8 and 12 days, respectively. This study showed that copper induced an oxidative stress in fish liver before significant metal accumulation in the liver could be detected, suggesting the involvement of differential mechanisms in copper uptake and metabolism. Three-spined stickleback appears to be a sensitive model to study oxidative stress induced by metals.

摘要

本研究旨在描述暴露于铜中的三刺鱼的生物标志物反应。为此,成年三刺鱼在硫酸铜中暴露 3 周,浓度分别为 0、25、100 和 200μgL(-1)作为 Cu。在第 4、8、12 和 21 天,测量了包括肝脏、性腺和脾脏体指数、肝生物标志物(过氧化氢酶 (CAT)、超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GPx)、谷胱甘肽 (GSH)、谷胱甘肽-S-转移酶 (GST) 和 7-乙氧基色原-O-去乙基酶 (EROD)) 和肝铜锌浓度在内的多个参数。暴露的前 8 天,铜迅速诱导抗氧化酶的短暂增加和谷胱甘肽含量的消耗。暴露 8 天和 12 天后,分别在两个较高的暴露浓度下观察到鱼肝脏中铜和锌的显著积累。本研究表明,在肝脏中可检测到明显的金属积累之前,铜诱导了鱼肝脏中的氧化应激,表明在铜的摄取和代谢中涉及不同的机制。三刺鱼似乎是研究金属诱导的氧化应激的敏感模型。

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