Zhang De Lu, Liu Si Yi, Zhang Jing, Hu Chun Xiang, Li Dun Hai, Liu Yong Ding
Department of Lifescience and Biotechnology, School of Chemistry, Chemical Engineering and Life Science, Wuhan University of Technology, Wuhan 430070, PR China.
Department of Lifescience and Biotechnology, School of Chemistry, Chemical Engineering and Life Science, Wuhan University of Technology, Wuhan 430070, PR China.
Ecotoxicol Environ Saf. 2015 Mar;113:425-32. doi: 10.1016/j.ecoenv.2014.12.029. Epub 2014 Dec 24.
Aphanizomenon flos-aquae secretes paralytic shellfish poisons (PSPs), termed aphantoxins, and endangers environmental and human health via eutrophication of water worldwide. Although the molecular mechanism of neuronal PSP toxicity has been well studied, several issues remain unresolved, notably the in vivo hepatic antioxidative responses to this neurotoxin. Aphantoxins extracted from a natural isolate of A. flos-aquae DC-1 were resolved by high performance liquid chromatography. The primary components were gonyautoxins 1 and 5 and neosaxitoxin. Zebrafish (Danio rerio) were treated intraperitoneally with either 5.3 or 7.61 (low and high doses, respectively) μg saxitoxin (STX) equivalents (eq)/kg of A. flos-aquae DC-1 aphantoxins. Antioxidative responses in zebrafish liver were examined at different timepoints 1-24h post-exposure. Aphantoxin administration significantly enhanced hepatic malondialdehyde (MDA) content 1-12h post-exposure, indicative of oxidative stress and lipid peroxidation. By contrast, levels of reduced glutathione (GSH) in zebrafish liver declined significantly after 3-24h exposure, suggesting that GSH participates in MDA metabolism. A significant upregulation of the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) was observed, suggesting that aphantoxins induce lipid peroxidation in zebrafish liver and are likely to be hepatotoxic. Hepatic levels of MDA and GSH, and of the three enzymes (SOD, CAT, and GPx), therefore provide potential biomarkers for studying environmental exposure to aphantoxins/PSPs from cyanobacterial blooms.
水华束丝藻分泌麻痹性贝类毒素（PSP），即水华毒素，通过全球水体富营养化危害环境和人类健康。尽管神经元PSP毒性的分子机制已得到充分研究，但仍有几个问题尚未解决，尤其是对这种神经毒素的体内肝脏抗氧化反应。从水华束丝藻DC-1的天然分离株中提取的水华毒素通过高效液相色谱法进行分离。主要成分是膝沟藻毒素1和5以及新石房蛤毒素。斑马鱼（Danio rerio）腹腔注射5.3或7.61（分别为低剂量和高剂量）μg石房蛤毒素（STX）当量（eq）/kg的水华束丝藻DC-1水华毒素。在暴露后1-24小时的不同时间点检测斑马鱼肝脏中的抗氧化反应。给予水华毒素后，暴露后1-12小时肝脏丙二醛（MDA）含量显著增加，表明存在氧化应激和脂质过氧化。相比之下，斑马鱼肝脏中还原型谷胱甘肽（GSH）水平在暴露3-24小时后显著下降，表明GSH参与MDA代谢。观察到超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPx）的活性显著上调，表明水华毒素在斑马鱼肝脏中诱导脂质过氧化，可能具有肝毒性。因此，肝脏中MDA和GSH的水平以及这三种酶（SOD、CAT和GPx）的水平为研究环境中蓝藻水华中水华毒素/PSP的暴露提供了潜在的生物标志物。
