A different sequence of events than previously reported leads to arsenic-induced damage in Ceratophyllum demersum L.
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.