Liang Ye, Chen Xinglan, Lu Xuxin, Jin Sichen, Min Yuanqi, Yang Jiaxin
Jiangsu Province Key Laboratory for Biodiversity & Biotechnology and Jiangsu Province Key Laboratory for Fisheries Live Food, School of Life Sciences, Nanjing Normal University, Nanjing 210023, PR China.
Jiangsu Province Key Laboratory for Biodiversity & Biotechnology and Jiangsu Province Key Laboratory for Fisheries Live Food, School of Life Sciences, Nanjing Normal University, Nanjing 210023, PR China.
Aquat Toxicol. 2017 Nov;192:78-88. doi: 10.1016/j.aquatox.2017.09.013. Epub 2017 Sep 14.
Toxicants released during the degradation of cyanobacterial blooms, such as microcystin-LR (MC-LR) and nitrite (NO-N), affect the growth of aquatic organisms. The freshwater rotifer Brachionus calyciflorus was exposed to solutions with different combined concentrations of MC-LR (0, 10, 50, 100, and 200μgL) and NO-N (0, 2, 4, 6, and 8mgL) to assess the combined effects of MC-LR and NO-N on life cycle parameters and oxidative stress. Single solutions of MC-LR 200μgL and NO-N 8mgL were toxic to rotifers. MC-LR combined with NO-N decreased population growth rate (r), survival, and reproduction, but increased reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) contents (p<0.01). Superoxide dismutase (SOD) and catalase (CAT) activities and mRNA expression levels of MnSOD, CuZnSOD, and CAT significantly decreased under high concentrations of MC-LR or NO-N (p<0.05). ROS levels had negative correlations with antioxidant enzyme activities and expression levels of antioxidant genes (p<0.01). MC-LR and NO-N had interactive effects on r, reproduction, ROS levels, MDA content, SOD activity, and expression levels of MnSOD and CAT (p<0.05). By contrast, these effects were antagonistic on survival, CAT activity, GSH content, and expression level of CuZnSOD (p>0.05). Results showed that cyanobacterial metabolites act synergistically and antagonistically to cause toxicity to B. calyciflorus. ROS-mediated toxicity was considered the mechanism by which MC-LR and NO-N induce damage.
蓝藻水华降解过程中释放的有毒物质,如微囊藻毒素-LR(MC-LR)和亚硝酸盐(NO-N),会影响水生生物的生长。将淡水轮虫萼花臂尾轮虫暴露于含有不同组合浓度的MC-LR(0、10、50、100和200μg/L)和NO-N(0、2、4、6和8mg/L)的溶液中,以评估MC-LR和NO-N对生命周期参数和氧化应激的联合影响。MC-LR 200μg/L和NO-N 8mg/L的单一溶液对轮虫有毒。MC-LR与NO-N联合降低了种群增长率(r)、存活率和繁殖率,但增加了活性氧(ROS)、丙二醛(MDA)和谷胱甘肽(GSH)含量(p<0.01)。在高浓度的MC-LR或NO-N作用下,超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性以及MnSOD、CuZnSOD和CAT的mRNA表达水平显著降低(p<0.05)。ROS水平与抗氧化酶活性和抗氧化基因表达水平呈负相关(p<0.01)。MC-LR和NO-N对r、繁殖、ROS水平、MDA含量、SOD活性以及MnSOD和CAT的表达水平具有交互作用(p<0.05)。相比之下,这些影响对存活率、CAT活性、GSH含量和CuZnSOD表达水平具有拮抗作用(p>0.05)。结果表明,蓝藻代谢产物通过协同和拮抗作用对萼花臂尾轮虫产生毒性。ROS介导毒性被认为是MC-LR和NO-N诱导损伤的机制。