Abstract：
The present study provides information on the effects of BPA on ROS production-related phenomena in the chlorophytes Ulva rigida and U. intestinalis, and on the mechanism they establish against BPA toxicity, at environmentally relevant concentrations (0.1-3 μg L-1). Up-regulated H2O2 generation seems to be a key factor causing oxidative damage. Interspecific differences, in terms of the mechanism and the temporal response to BPA toxicity were observed. BPA effects on U. rigida were more intense and appeared earlier (on 1D at 0.1 μg L-1) compared to U. intestinalis and mostly after 7D (LOEC: 0.3 μg L-1, Terminal time, Tt: 7D). In U. rigida, on 1-5D, the \'mosaic\' type effect patterns (\'models\' 3A/3B) with \'unaffected\' and \'affected\' areas (dark content, positive H2DCF-DA staining signal/H2O2 production and chlorophyll autofluorescence signal loss) indicated a time-dependent manner. After 7D, only U. rigida cells with dark content formed aggregates, showing positive H2O2 production (\'model\' 4) or in some cells oxidative damages triggering retrograde signaling in the neighboring \'unaffected\' areas (\'model\' 5). H2O2 overproduction (CTCF ratio) in U. rigida, on 1D at the lowest concentration and after 7D at 0.3-1/3 μg L-1, respectively, seems to stimulate (poly)phenolic production, in a dose- and time-dependent manner. U. intestinalis did not display severe BPA impact (i.e., \'models\' 4, 5) at any exposures, although at a later time indicated a lower LOEC (0.1 μg L-1, Tt: 9D) than that in U. rigida. In U. intestinalis, H2O2 production does not appear to stimulate high (poly)phenolic amounts.
摘要：
本研究提供了有关BPA对绿藻Ulva刚性和U.testinalis中ROS产生相关现象的影响的信息，以及它们建立的对抗BPA毒性的机制，在环境相关浓度（0.1-3μgL-1）。H2O2生成上调似乎是引起氧化损伤的关键因素。种间差异,在机制和对BPA毒性的时间反应方面进行了观察。与肠杆菌相比，BPA对硬藻的影响更强烈，并且出现更早（在0.1μgL-1的1D），并且大部分在7D后（LOEC：0.3μgL-1，终止时间，Tt:7D)。在美国，在1-5D，\'mosaic\'typeeffectpatterns(\'models\'3A/3B)with\''unaffecting\'and\'affected\'area(darkcontent,H2DCF-DA染色阳性信号/H2O2产生和叶绿素自发荧光信号损失）表明时间依赖性。7D后,只有具有深色内容物的刚性芽孢杆菌细胞形成聚集体，显示H2O2产生阳性（\'模型\'4）或在某些细胞中的氧化损伤触发邻近\'未受影响\'区域的逆行信号（\'模型\'5）。刚性美国的H2O2过量生产(CTCF比率)，在最低浓度的1D和在0.3-1/3μgL-1的7D后，似乎刺激了(聚)酚的生产，以剂量和时间依赖的方式。肠杆菌没有表现出严重的BPA影响(即，\'模型\'4，5)在任何暴露下，尽管在以后的时间表明LOEC（0.1μgL-1，Tt：9D）低于刚性美国。在肠杆菌中，H2O2的产生似乎不刺激高(多)酚量。
