Nanjing Institute of Environmental Sciences, Key Laboratory of Pesticide Environmental Assessment and Pollution Control, Ministry of Environmental Protection, Nanjing 210042, PR China.
Comp Biochem Physiol C Toxicol Pharmacol. 2012 Apr;155(3):483-90. doi: 10.1016/j.cbpc.2011.12.008. Epub 2011 Dec 31.
Microcystin-LR (MC-LR) produced by cyanobacteria are potent specific hepatotoxins. So far the pathogenesis of environmental MC-LR toxicity to aquatic organisms has not been fully elucidated. In the present study the accumulation of MC-LR was investigated in various organs/tissues of Cyprinus carpio L. (C. carpio) following exposure to MC-LR for 14 d at environmentally relevant concentrations (0.1 to 10 μg L(-1)). Results showed that the presence of MC-LR enhanced toxin accumulation in all investigated organs and the highest accumulation was found in the liver of fish exposed to 5.0 μg L(-1) of MC-LR. An EPR analysis indicated ·OH intensity in liver was significantly induced at 0.1 μg L(-1) of MC-LR and then restored when the MC-LR concentration was greater than 0.1 μg L(-1). After 14-day exposure, MC-LR (1.0-10.0 μg L(-1) of MC-LR) caused a pronounced promotion of glutathione S-transferase (GST) activity and a depletion of reduced glutathione (GSH) content in fish liver, which indicated that GSH was involved in detoxification of MC-LR and the conjugation reaction of MC-LR and GSH occurred. A mild oxidative damage was evidenced by the accumulation of malondialdehyde (MDA) level at 5.0 μg L(-1) of MC-LR exposure, but which was restored when the MC-LR concentration was increased to 10.0 μg L(-1). The responses of antioxidant enzymes and the induction of HSP70 expression might contribute to MC-LR tolerance of C. carpio. However, the protein phosphatase (PP) activities were strikingly inhibited in all treated groups. Thus, the overall toxicity of environmental MC-LR on C. carpio seems to be initiated in the liver via both the ROS pathway and the PP inhibition pathway, and the latter might be more important when ambient MC-LR concentration is greater than 0.1 μg L(-1). More importantly, these results can help to support the evaluation on the potential effects of MC-LR under common environmental concentrations.
微囊藻毒素-LR（MC-LR）是由蓝藻产生的强效特异性肝毒素。到目前为止，环境中 MC-LR 对水生生物的毒性的发病机制尚未完全阐明。在本研究中，在与环境相关的浓度（0.1 至 10μg/L）下，用 MC-LR 处理 14 天后，研究了 MC-LR 在鲤鱼（C. carpio）的各种器官/组织中的积累情况。结果表明，MC-LR 的存在增强了所有研究器官中毒素的积累，在暴露于 5.0μg/L MC-LR 的鱼的肝脏中发现了最高的积累。EPR 分析表明，在 0.1μg/L MC-LR 时，肝脏中·OH 强度显著诱导，然后当 MC-LR 浓度大于 0.1μg/L 时恢复。经过 14 天暴露，MC-LR（1.0-10.0μg/L 的 MC-LR）导致鱼肝脏中的谷胱甘肽 S-转移酶（GST）活性显著促进和还原型谷胱甘肽（GSH）含量耗尽，这表明 GSH 参与了 MC-LR 的解毒和 MC-LR 与 GSH 的共轭反应。在 5.0μg/L MC-LR 暴露时，丙二醛（MDA）水平的积累表明存在轻度氧化损伤，但当 MC-LR 浓度增加到 10.0μg/L 时，这种损伤得到恢复。抗氧化酶的反应和 HSP70 表达的诱导可能有助于鲤鱼对 MC-LR 的耐受。然而，在所有处理组中，蛋白磷酸酶（PP）活性都被显著抑制。因此，环境中 MC-LR 对鲤鱼的整体毒性似乎是通过 ROS 途径和 PP 抑制途径在肝脏中引发的，当环境 MC-LR 浓度大于 0.1μg/L 时，后者可能更为重要。更重要的是，这些结果可以帮助支持在常见环境浓度下对 MC-LR 潜在影响的评估。
