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实验暴露于镍的日本虎头海狮中氧化损伤的影响。

Oxidative damage effects in the copepod Tigriopus japonicus Mori experimentally exposed to nickel.

机构信息

College of Oceanography and Environmental Science, State Key Laboratory of Marine Environmental Science, Xiamen University, 361005, Xiamen, People's Republic of China.

出版信息

Ecotoxicology. 2010 Feb;19(2):273-84. doi: 10.1007/s10646-009-0410-6. Epub 2009 Sep 26.

DOI:10.1007/s10646-009-0410-6
PMID:19821026
Abstract

Tigriopus japonicus Mori has been recognized as a good model for toxicological testing of marine pollutants. Recently, a large number of genes have been identified from this copepod, and their mRNA expression has been studied independently against exposure to marine pollutants; however, biochemical-response information is relatively scarce. The response of T. japonicus to nickel (Ni) additions was examined under laboratory-controlled conditions in 12 days exposure. Superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), acetylcholinesterase (AchE), reduced glutathione (GSH), the ratio of reduced to oxidized glutathione (GSH/GSSG) and metallothionein (MT) were analyzed for Ni treatments (0, 0.125, 0.25, 0.75 and 3.0 mg/L) after 1, 4, 7 and 12 days. The thiobarbituric reactive species assay was used to evaluate lipid peroxidation (LPO) level in copepods after exposure. The results showed that Ni remarkably affected the biochemical parameters (SOD, GPx, GST, GSH, and GSH/GSSG) after certain exposure durations. However, the copepod's LPO level was significantly decreased under metal treatments after exposure, hinting that the factors involved in LPO might not significantly depend on the operations and functions in the antioxidant system. Ni exhibited the neurotoxicity to copepods, because its use obviously elevated AchE activity. During exposure, Ni initially displayed an inhibition effect but induced MT synthesis in T. japonicus by day 12, probably being responsible for metal detoxification. Thus, Ni had intervened in the detoxification process and antioxidant system of this copepod, and it could be used as a suitable bioindicator of Ni exposure via measuring SOD, GPx, GST, and MT as biomarkers.

摘要

日本虎头海葵已被公认为海洋污染物毒理学测试的良好模型。最近,从这种桡足类动物中鉴定出了大量基因,并针对暴露于海洋污染物的情况独立研究了它们的 mRNA 表达;然而,生化反应信息相对较少。在实验室控制条件下,用 12 天的时间来检测日本虎头海葵对镍(Ni)添加的反应。在 1、4、7 和 12 天的时间点,对 Ni 处理(0、0.125、0.25、0.75 和 3.0 mg/L)的超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)、谷胱甘肽-S-转移酶(GST)、乙酰胆碱酯酶(AchE)、还原型谷胱甘肽(GSH)、还原型与氧化型谷胱甘肽(GSH/GSSG)和金属硫蛋白(MT)进行了分析。用硫代巴比妥酸反应物质测定法评估暴露后桡足类动物的脂质过氧化(LPO)水平。结果表明,Ni 在一定暴露时间后显著影响生化参数(SOD、GPx、GST、GSH 和 GSH/GSSG)。然而,暴露后金属处理使桡足类动物的 LPO 水平显著降低,表明 LPO 涉及的因素可能不明显依赖于抗氧化系统的运作和功能。Ni 对桡足类动物表现出神经毒性,因为它明显增加了 AchE 活性。在暴露期间,Ni 最初表现出抑制作用,但在第 12 天诱导了 T. japonicus 中 MT 的合成,可能是为了进行金属解毒。因此,Ni 干预了这种桡足类动物的解毒过程和抗氧化系统,并且可以通过测量 SOD、GPx、GST 和 MT 作为生物标志物来作为 Ni 暴露的合适生物标志物。

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