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用重铬酸盐(VI)处理的鱼(欧鳗)肝脏中顺磁铬的 EPR 检测及相关氧化应激反应——对阐明毒性机制的贡献。

EPR detection of paramagnetic chromium in liver of fish (Anguilla anguilla) treated with dichromate(VI) and associated oxidative stress responses-contribution to elucidation of toxicity mechanisms.

机构信息

Biology Department of the University of Aveiro & CESAM, 3810-193 Aveiro, Portugal.

出版信息

Comp Biochem Physiol C Toxicol Pharmacol. 2013 Mar;157(2):132-40. doi: 10.1016/j.cbpc.2012.10.009. Epub 2012 Nov 6.

DOI:10.1016/j.cbpc.2012.10.009
PMID:23142145
Abstract

The impact of chromium (Cr) on fish health has been the subject of numerous investigations, establishing a wide spectrum of toxicity, attributed particularly to the hexavalent form [Cr(VI)]. However, reports on the simultaneous assessment of Cr toxicity in fish and its toxico-kinetics, namely involving metal speciation, are scarce. Therefore, keeping in view the understanding of the mechanisms of Cr(VI) toxicity, this work intended to detect the formation of paramagnetic Cr species in liver of Anguilla anguilla following short-term dichromate(VI) intraperitoneal treatment (up to 180 min), assessing simultaneously the pro-oxidant properties. The formation of Cr(V) and Cr(III) was examined by electron paramagnetic resonance (EPR), as an innovative approach in the context of fish toxicology, and related with the levels of total Cr. Cr(V) was successfully detected and quantified by EPR spectrometry, showing a transient occurrence, mostly between 15 and 90 min post-injection, with a peak at 30 min. The limitations of EPR methodology towards the detection and quantification of Cr(III) were confirmed. Although Cr(VI) exposure induced the antioxidant system in the eel's liver, the oxidative deterioration of lipids was not prevented. Overall, the results suggested that Cr(V), as a short-lived species, did not appear to be directly and primarily responsible for the cellular damaging effects observed, since stress responses persisted up to the end of exposure regardless Cr(V) drastic decay. Though further research is needed, ROS mediated pathways (suggested by superoxide dismutase and catalase activity induction) and formation of Cr(III) complexes emerged as the most plausible mechanisms involved in Cr(VI) toxicity.

摘要

铬(Cr)对鱼类健康的影响一直是众多研究的主题,确立了广泛的毒性,特别是归因于六价形式[Cr(VI)]。然而,关于同时评估鱼类中 Cr 的毒性及其毒代动力学(即涉及金属形态)的报告很少。因此,鉴于了解 Cr(VI)毒性的机制,本工作旨在检测短时间内(长达 180 分钟)腹腔内 Cr(VI)处理后,欧鳗肝脏中顺磁 Cr 物种的形成,同时评估其促氧化特性。通过电子顺磁共振(EPR)检查 Cr(V)和 Cr(III)的形成,这是鱼类毒理学背景下的一种创新方法,并与总 Cr 水平相关。通过 EPR 光谱成功检测和定量 Cr(V),表明其短暂存在,主要在注射后 15 至 90 分钟之间,在 30 分钟时达到峰值。EPR 方法检测和定量 Cr(III)的局限性得到了证实。尽管 Cr(VI)暴露诱导了鳗鱼肝脏中的抗氧化系统,但并未防止脂质的氧化恶化。总的来说,结果表明,作为一种短寿命的物种,Cr(V)似乎不是导致观察到的细胞损伤的直接和主要原因,因为无论 Cr(V)急剧衰减如何,应激反应仍持续到暴露结束。尽管需要进一步研究,但 ROS 介导的途径(通过超氧化物歧化酶和过氧化氢酶活性诱导表明)和 Cr(III)配合物的形成被认为是参与 Cr(VI)毒性的最可能机制。

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