Mechanism of long-term toxicity of CuO NPs to microalgae.

Little is known regarding the detailed mechanism of CuO NPs' toxicity to microalgal primary metabolism pathway. Photosynthesis and respiration are the most important primary metabolism and the main sources of production of reactive oxygen species (ROS), but the effect of CuO NPs on both of them has not been systematically studied to date. Our research demonstrated that long-term treatment with CuO NPs significantly inhibited activities of photosynthesis and respiration in microalgae, and the photosynthesis was more sensitive to the toxicity of CuO NPs than respiration. CuO NPs could be absorbed by microalgae and be converted into Cu2O NPs concentrated in chloroplast. The internalized Cu, regardless of whether the exposure was Cu2+ or CuO NPs had the same capacity to damage chloroplast structure. The result also shows that the oxygen-evolving complex (OEC) in the photosynthetic electron transport chain was the most sensitive site to CuO NPs and Cu2+-treated microalgae had the same damage site as that of CuO NPs, which may be related to the Mn cluster that is dissociated by Cu ions released from CuO NPs. The damage of OEC inhibited photosynthetic electron transport to increase excess excited energy, which caused the accumulation of ROS in chloroplast. The accumulation of ROS damaged the structure of cell membrane and aggravated the PSII photoinhibition, further decreasing the efficiency of light energy utilization. In conclusion, the Cu ionic toxicity of photosynthetic apparatus by CuO NPs resulted in the carbon starvation and the accumulation of ROS to inhibit the growth of microalgae.