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首页> 外文期刊>Mutation Research: International Journal on Mutagenesis, Chromosome Breakage and Related Subjects >Oxidative stress and genotoxic effects in gill and kidney of Anguilla anguilla L. exposed to chromium with or without pre-exposure to beta-naphthoflavone.
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Oxidative stress and genotoxic effects in gill and kidney of Anguilla anguilla L. exposed to chromium with or without pre-exposure to beta-naphthoflavone.

机译:在暴露或未暴露于β-萘黄酮的情况下,暴露于铬的安圭拉鳗g和肾脏的氧化应激和遗传毒性作用。

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Fish in the aquatic environment can be subjected to a multipollution state and the occurrence of sequential exposures is an important aspect of eco-toxicological research. In this context, a preceding exposure can affect a toxic response to a subsequent exposure. Therefore, the current study was based on sequential exposures, viz. to a PAH-like compound (beta-naphthoflavone, BNF) followed by a heavy metal (chromium, Cr), focusing on the assessment of oxidative stress responses and their role in induction of genotoxicity. Oxidative stress responses in gill and kidney were investigated in European eel (Anguilla anguilla L.), and measured as lipid peroxidation (LPO), glutathione peroxidase (GPX), catalase (CAT) and glutathione S-transferase (GST) activity, and reduced glutathione (GSH) concentration, whereas genotoxicity was measured as DNA strand breakage. Fish were exposed for 24 h to two Cr concentrations (100 microM, 1 mM), with or without pre-exposure to BNF (2.7 microM, 24 h). In gill, a GSH decrease was observed along with loss of DNA integrity at all exposure conditions except at the lowest Cr concentration, showing a crucial role of GSH over genotoxicity. Moreover, sporadic induction of antioxidant enzymes was not effective in the protection against genotoxicity. However, a different mechanism seems to occur in kidney, since the loss of DNA integrity detected for all exposed groups was not accompanied by alterations in antioxidant levels. With regards to peroxidative damage, both organs showed an LPO increase after sequential exposure to BNF and 100 microM Cr. However, no association between LPO induction and antioxidant responses could be established, showing that LPO is not predictable solely on the basis of antioxidant depletion. The interference of BNF pre-exposure with the response of organs to Cr showed a marked dependence on the Cr concentration. Gill showed synergistic effects on LPO and GPX increase, as well as on CAT and GSH decrease for the lowest Cr concentration. However, for the highest concentration an additive effect on decrease of DNA integrity and an antagonistic effect on the increase of GPX were observed. In kidney, synergistic effects were evident on LPO increase and GSH decrease for the lowest Cr concentration, as well as on CAT and GST decrease for the highest concentration. In contrast, an antagonistic action was observed on DNA integrity loss for both Cr concentrations. The current results are relevant in assessing the interactions of PAHs and metals and contribute to a better knowledge about oxidative stress and mechanisms of genotoxicity in fish.
机译:水生环境中的鱼类可能会处于多重污染状态,并且顺序暴露是生态毒理学研究的重要方面。在这种情况下,先前的暴露会影响对后续暴露的毒性反应。因此,当前的研究是基于连续暴露的。首先是PAH样化合物(β-萘黄酮,BNF),然后是重金属(铬,Cr),重点是评估氧化应激反应及其在诱导遗传毒性中的作用。在欧洲鳗鱼(Anguilla anguilla L.)中研究了g和肾脏的氧化应激反应,并以脂质过氧化(LPO),谷胱甘肽过氧化物酶(GPX),过氧化氢酶(CAT)和谷胱甘肽S-转移酶(GST)活性进行了测定,并降低了谷胱甘肽(GSH)浓度,而遗传毒性以DNA链断裂来衡量。将鱼暴露于两种Cr浓度(100 microM,1 mM)中24小时,有或没有预先暴露于BNF(2.7 microM,24 h)。在g中,除最低的Cr浓度外,在所有暴露条件下均观察到GSH的降低以及DNA完整性的丧失,这表明GSH在遗传毒性方面起着至关重要的作用。此外,零星地诱导抗氧化酶不能有效地防止遗传毒性。然而,似乎在肾脏中发生了不同的机制,因为在所有暴露的组中检测到的DNA完整性丧失并没有伴随着抗氧化剂水平的改变。关于过氧化损伤,在连续暴露于BNF和100 microM Cr后,两个器官均显示LPO增加。但是,无法确定LPO诱导与抗氧化剂反应之间的关联,这表明LPO不能仅基于抗氧化剂的消耗来预测。 BNF预暴露对器官对Cr反应的干扰显示出对Cr浓度的显着依赖性。吉尔在最低的铬浓度下对LPO和GPX升高,对CAT和GSH降低具有协同作用。然而,对于最高浓度,观察到对DNA完整性降低的加和作用以及对GPX增加的拮抗作用。在肾脏中,对于最低的Cr浓度,LPO升高和GSH降低具有协同作用,而对于最高浓度的CAT和GST则具有协同作用。相反,在两种Cr浓度下都观察到对DNA完整性丧失的拮抗作用。目前的结果与评估多环芳烃和金属的相互作用有关,有助于更好地了解鱼类的氧化应激和遗传毒性机理。

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