Li Xiaoyu, Liu Yongding, Song Lirong, Liu Jiantong
College of Life Science, Henan Normal University, Xinxiang, Henan 453002, People's Republic of China.
Toxicon. 2003 Jul;42(1):85-9. doi: 10.1016/s0041-0101(03)00104-1.
The freshwater, bloom-forming cyanobacterium (blue-green alga) Microcystis aeruginosa produces a peptide hepatotoxin, which causes the damage of animal liver. Recently, toxic Microcystis blooms frequently occur in the eutrophic Dianchi Lake (300 km2 and located in the South-Western of China). Microcystin-LR from Microcystis in Dianchi was isolated and purified by high performance liquid chromatography (HPLC) and its toxicity to mouse and fish liver was studied (Li et al., 2001). In this study, six biochemical parameters (reactive oxygen species, glutathione, superoxide dismutase, catalase, glutathione peroxide and glutathione S-transferase) were determined in common carp hepatocytes when the cells were exposed to 10 microg microcystin-LR per litre. The results showed that reactive oxygen species (ROS) contents increased by more than one-time compared with the control after 6 h exposure to the toxin. In contrast, glutathione (GSH) levels in the hepatocytes exposed to microcystin-LR decreased by 47% compared with the control. The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxide (GSH-Px) increased significantly after 6 h exposure to microcystin-LR, but glutathione S-transferase (GST) activity showed no difference from the control. These results suggested that the toxicity of microcystin-LR caused the increase of ROS contents and the depletion of GSH in hepatocytes exposed to the toxin and these changes led to oxidant shock in hepatocytes. Increases of SOD, CAT and GSH-Px activities revealed that these three kinds of antioxidant enzymes might play important roles in eliminating the excessive ROS. This paper also examined the possible toxicity mechanism of microcystin-LR on the fish hepatocytes and the results were similar to those with mouse hepatocytes.
淡水蓝藻水华形成的铜绿微囊藻会产生一种肽类肝毒素，可导致动物肝脏损伤。近年来，富营养化的滇池（面积300平方公里，位于中国西南部）频繁出现有毒微囊藻水华。采用高效液相色谱法（HPLC）从滇池微囊藻中分离纯化出微囊藻毒素-LR，并研究了其对小鼠和鱼肝的毒性（Li等人，2001年）。在本研究中，将鲤鱼肝细胞暴露于每升10微克微囊藻毒素-LR中，测定了六个生化参数（活性氧、谷胱甘肽、超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽S-转移酶）。结果显示，毒素暴露6小时后，活性氧（ROS）含量比对照组增加了一倍多。相比之下，暴露于微囊藻毒素-LR的肝细胞中谷胱甘肽（GSH）水平比对照组降低了47%。暴露于微囊藻毒素-LR 6小时后，超氧化物歧化酶（SOD）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GSH-Px）的活性显著增加，但谷胱甘肽S-转移酶（GST）活性与对照组无差异。这些结果表明，微囊藻毒素-LR的毒性导致暴露于毒素的肝细胞中ROS含量增加和GSH消耗，这些变化导致肝细胞氧化应激。SOD、CAT和GSH-Px活性的增加表明这三种抗氧化酶可能在消除过量ROS中发挥重要作用。本文还研究了微囊藻毒素-LR对鱼肝细胞的可能毒性机制，结果与小鼠肝细胞相似。
