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镉暴露后线粒体基因表达、抗氧化反应和组织病理学变化。

Mitochondrial gene expression, antioxidant responses, and histopathology after cadmium exposure.

机构信息

Laboratory of Radioecology and Ecotoxicology (LRE), Institute of Radioprotection and Nuclear Safety (IRSN), Bd 186, BP 3, 13115 Saint-Paul-Lez-Durance, France; Laboratory of Aquatic Ecotoxicology (EA), University of Bordeaux1/UMR CNRS 5805, Dr Peyneau Square, 33120 Arcachon, France.

出版信息

Environ Toxicol. 2014 Aug;29(8):893-907. doi: 10.1002/tox.21817. Epub 2012 Oct 15.

Abstract

The present study investigates cadmium effects on the transcription of mitochondrial genes of Procambarus clarkii after acute (0.05, 0.5, and 5 mg Cd/L; 4-10 days) and chronic exposures (10 μg Cd/L; 30-60 days). Transcriptional responses of cox1, atp6, and 12S using quantitative real-time RT-PCR were assessed in gills and hepatopancreas. Additionally, the expression levels of genes involved in detoxification and/or oxidative stress responses [mt, sod(Mn)] and enzymatic activities of antioxidants (SOD, CAT, GPX, and GST) were analyzed. The histopathological effects in hepatopancreas of crayfish were evaluated by light microscopy. Relationships between endpoints at different levels of biological organization and Cd bioaccumulation were also examined. Cd induced high levels of bioaccumulation, which was followed by mitochondrial dysfunction and histological alterations in both experiments. Moreover, perturbations in the defence mechanisms against oxidative stress tended to increase with time. Results also showed that molecular responses can vary depending on the intensity and duration of the chemical stress applied to the organisms and that the study of mt gene expression levels seemed to be the best tool to assess Cd intoxication.

摘要

本研究调查了镉对克氏原螯虾(Procambarus clarkii)线粒体基因转录的急性(0.05、0.5 和 5mg Cd/L;4-10 天)和慢性暴露(10μg Cd/L;30-60 天)的影响。使用定量实时 RT-PCR 评估了cox1、atp6 和 12S 在鳃和肝胰腺中的转录反应。此外,还分析了参与解毒和/或氧化应激反应的基因(mt、sod(Mn))的表达水平以及抗氧化剂(SOD、CAT、GPX 和 GST)的酶活性。通过光镜评估了螯虾肝胰腺的组织病理学效应。还检查了不同水平的生物组织终点与 Cd 生物累积之间的关系。在这两个实验中,镉都引起了高水平的生物累积,随后导致了线粒体功能障碍和组织学改变。此外,对抗氧化应激的防御机制的干扰似乎随着时间的推移而增加。结果还表明,分子反应可能因施加给生物体的化学应激的强度和持续时间而异,并且研究 mt 基因表达水平似乎是评估 Cd 中毒的最佳工具。

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