A different sequence of events than previously reported leads to arsenic-induced damage in Ceratophyllum demersum L.
A different sequence of events than previously reported leads to arsenic-induced damage in Ceratophyllum demersum L.
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DOI：
10.1039/c3mt00317e
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发表时间：
2014-02
期刊：
影响因子：
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通讯作者：
Seema Mishra-;H. Stärk;H. Küpper
中科院分区：
文献类型：
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作者：
Seema Mishra-;H. Stärk;H. Küpper
砷 (As) 是一种常见的污染物，在植物环境相关条件下，砷的毒性机制仍然存在许多问题。在这里，我们研究了各种提议的砷毒性机制的阈值和相互作用。在与环境相关的条件下，在无根水生植物金鱼藻（植物芽的模型）中进行了实验。砷（以 As(v) 形式提供）以低得多的浓度抑制植物代谢，且事件顺序与之前报道的不同。第一个观察到的毒性效应是色素浓度降低，甚至在 0.5 μM As 时也开始出现这种效应。与有毒金属相反，在亚致死浓度的 As 浓度下，未发现光系统 II 反应中心（PSIIRC；以 Fv/Fm 测量）受到抑制。相反，光捕获色素的减少导致激子向 PSIIRC 的转移效率降低。当砷浓度较高时，光捕获复合物 II (LHCII) 会导致非光化学猝灭 (NPQ) 增加。此后，光合电子传递下降，但淀粉含量增加，表明对淀粉消耗的抑制作用强于对淀粉生产的抑制作用。在致死的砷浓度下，光合作用被完全抑制，其故障导致氧化应激，而不是之前报道的相反。在观察到任何氧化应激迹象之前，光合作用就受到抑制。磷酸盐升高极大地改变了致命砷效应的阈值，这不仅是通过已知的摄取竞争，而且还通过改变摄取调节和细胞内过程。
Arsenic (As) is a common pollutant, and still many questions remain concerning As toxicity mechanisms under environmentally relevant conditions in plants. Here we investigated thresholds and interactions of various proposed As toxicity mechanisms. Experiments were done under environmentally pertinent conditions in the rootless aquatic macrophyte Ceratophyllum demersum L., a model for plant shoots. Arsenic (provided as As(v)) inhibited plant metabolism at much lower concentrations and with a different sequence of events than previously reported. The first observed effect of toxicity was a decrease in pigment concentration, it started even at 0.5 μM As. In contrast to toxic metals, no inhibition of the photosystem II reaction centre (PSIIRC; measured as Fv/Fm) was found at sublethal As concentrations. Instead, the decrease in light harvesting pigments caused a less efficient exciton transfer towards the PSIIRC. At higher As concentrations this led to increased non-photochemical quenching (NPQ) by light harvesting complex II (LHCII). Afterwards, photosynthetic electron transport decreased, but the increase in starch content indicated stronger inhibition of starch consumption than production. At lethal As concentration, photosynthesis was completely inhibited, its malfunction caused oxidative stress and not the other way round as reported previously. Photosynthesis was inhibited before any sign of oxidative stress was observed. Elevated phosphate drastically shifted thresholds of lethal As effects, not only by the known uptake competition but also by modifying uptake regulation and intracellular processes.