Laboratory of Animal Physiology, Zoology Department, School of Biology, Faculty of Science, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece.
University of Bologna, Interdepartment Centre for Environmental Science Research, via S. Alberto 163, 48123 Ravenna, Italy.
Aquat Toxicol. 2014 Jan;146:186-95. doi: 10.1016/j.aquatox.2013.11.005. Epub 2013 Nov 15.
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 of Mytilus galloprovincialis hemocytes 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 mussel M. galloprovincialis hemocytes. 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 (PI3K) 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, Ca(2+)-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.
本研究旨在确定并比较暴露于雌激素 17β-雌二醇和金属镉对贻贝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。此外，研究这些参数是否可以构成水生污染监测的生物标志物也很有意义。我们的结果表明，微摩尔浓度的镉或 17β-雌二醇通过调节贻贝血细胞的氧化参数和抗氧化酶基因表达来影响贻贝的氧化还原状态。具体而言，我们的结果表明，用 5 μM 的氯化镉或 25 nM 的 17β-雌二醇处理血细胞 30 分钟会导致 ROS 产生显著增加；这导致了氧化损伤，表现为 DNA 损伤、蛋白质羰基化和脂质过氧化显著增加，以及抗氧化酶过氧化氢酶 (CAT)、超氧化物歧化酶 (SOD) 和谷胱甘肽 S-转移酶 (GST) 的 mRNA 水平增加。此外，我们的结果表明，镉或 17β-雌二醇信号通过已经已知的途径之一介导，该途径由磷脂酰肌醇 3-激酶 (PI3K) 启动，可能通过蛋白激酶 C (PKC) 到达 Na(+)/H(+) 交换器 (NHE)，或者通过涉及大多数情况下 NHE、PKC、Ca(2+)-依赖性 PKC 同工型、PI3-K、NADPH 氧化酶、一氧化氮 (NO) 合酶、c-Jun N-末端激酶 (JNK) 和环腺苷酸-3'-5'-单磷酸 (cAMP) 的激酶介导的信号通路介导。我们的结果还归因于 cAMP 的保护作用，因为预先升高的细胞内 cAMP 水平抑制了每种暴露诱导的信号。最后，由于水生无脊椎动物一直是海洋环境中污染影响评估最广泛使用的监测生物，并且考虑到所研究参数之间获得的正相关关系，我们可以建议同时使用这些氧化应激参数，在水生环境的生物监测中提供有效的早期预警系统。
