Oxidative stress parameters induced by exposure to either cadmium or 17β-estradiol on Mytilus galloprovincialis hemocytes. The role of signaling molecules.
Oxidative stress parameters induced by exposure to either cadmium or 17β-estradiol on Mytilus galloprovincialis hemocytes. The role of signaling molecules.
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DOI：
10.1016/j.aquatox.2013.11.005
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发表时间：
2014
影响因子：
4.5
通讯作者：
S. Koutsogiannaki;S. Franzellitti;E. Fabbri;M. Kaloyianni
中科院分区：
文献类型：
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作者：
S. Koutsogiannaki;S. Franzellitti;E. Fabbri;M. Kaloyianni
本研究的目的是确定和比较暴露于雌激素17β-雌二醇和金属镉对贻贝（Mytilus galloprovincia）血细胞氧化参数的可能影响，并阐明可能介导这两种化学物质所产生的研究效应的信号通路。研究结果表明，微摩尔浓度的镉或17β-雌二醇通过调节贻贝的氧化参数和抗氧化酶基因表达，影响贻贝的氧化还原状态。galloprovincialisemocytes.特别是，我们的研究结果表明，用5 μM氯化镉或25 nM 17β-雌二醇处理血细胞30分钟，可显著增加ROS的产生;这导致氧化损伤，例如显著增加的DNA损伤、蛋白质羰基化和脂质过氧化，以及抗氧化酶过氧化氢酶（CAT）的mRNA水平增加，超氧化物歧化酶（SOD）和谷胱甘肽S-转移酶（GST）。此外，我们的研究结果表明，镉或17β-雌二醇信号要么是通过一种已知的途径介导的，该途径由磷脂酰肌醇3-激酶（PI 3 K）启动并可能通过蛋白激酶C（PKC）到达Na+/H+交换器（NHE），要么是通过一种激酶介导的信号途径介导的，在大多数情况下，该途径涉及NHE、PKC、Ca 2+依赖的PKC亚型、PI 3-K、NADPH氧化酶、一氧化氮（NO）合酶、c-Jun氨基末端激酶（JNK）和环腺苷酸（cAMP）。我们的研究结果还归因于cAMP的保护作用，因为预先升高的细胞内cAMP水平抑制了每次暴露诱导的信号。最后，由于水生无脊椎动物一直是最广泛使用的监测生物在海洋环境中的污染影响评价，并考虑到所研究的参数之间的正相关性，我们可以建议同时使用这些氧化应激参数提供了一个有效的预警系统，在生物监测的水生环境。
The aim of the present study was to determine and compare the possible effects of exposure to an estrogen, 17β-estradiol and to a metal, cadmium on oxidative parameters ofMytilus galloprovincialishemocytes and to elucidate the signaling pathways that probably mediate the studied effects exerted by these two chemicals. In addition, it was of interest to investigate if the studied parameters could constitute biomarkers for aquatic pollution monitoring.Our results suggest that micromolar concentrations of either cadmium or 17β-estradiol affected the redox status of mussels by modulating oxidative parameters and antioxidant enzymes gene expression in musselM. galloprovincialishemocytes. In particular, our results showed that treatment of hemocytes with either 5 μM of cadmium chloride or with 25 nM of 17β-estradiol for 30 min caused significant increased ROS production; this led to oxidative damage exemplified by significant increased DNA damage, protein carbonylation and lipid peroxidation, as well as increased mRNA levels of the antioxidant enzymes catalase (CAT), superoxide dismoutase (SOD) and glutathione S-transferase (GST). Furthermore, our results suggest that either cadmium or 17β-estradiol signal is mediated either through one of the already known pathways initiated by photatidyl-inositol 3-kinase (PI3 K) and reaching Na+/H+exchanger (NHE) probably through protein kinase C (PKC) or a kinase-mediated signaling pathway that involves in most of the cases NHE, PKC, Ca2+-dependent PKC isoforms, PI3-K, NADPH oxidase, nitric oxide (NO) synthase, c-Jun N-terminal kinase (JNK) and cyclic adenosine-3′-5′-monophosphate (cAMP). Our results also attribute a protective role to cAMP, since pre-elevated intracellular cAMP levels inhibited the signal induced by each exposure. Finally, since aquatic invertebrates have been the most widely used monitoring organisms for pollution impact evaluation in marine environments and taking under consideration the positive correlation obtained between the studied parameters, we can suggest the simultaneous use of these oxidative stress parameters offering an effective early warning system in biomonitoring of aquatic environments.