Cell membrane damage induced by continuous stress of artemisinin sustained-release microspheres (ASMs) on Microcystis aeruginosa at different physiological stages.

Artemisinin sustained-release microspheres (ASMs) with long-term inhibition effects (> 40 days) on harmful freshwater bloom-forming cyanobacteria have been found in previous studies, but the inhibition mechanism is not completely clear. In the present study, we examined the growth effect of ASMs on Microcystis aeruginosa (M. aeruginosa) cells at different physiological stages. Growth experiments indicated that M. aeruginosa of different initial densities could be inhibited immediately and chlorophyll-a content both showed significant decreases following exposure of cyanobacteria to optimal dosage of ASMs for 20 days. The algicidal mechanism of ASMs was tested through a suite of physiological parameters (membrane permeability, antioxidant enzymes activity, and lipid peroxidation). The rise of cell membrane permeability indices (intracellular protein, nucleic acid contents, and conductivity) showed that the cellular membrane structure of M. aeruginosa was attacked by ASMs directly causing the leakage of cytoplasm. Antioxidant enzyme activity was a sensitive indicator of the impacts of ASMs which showed a significant downtrend after a few days. ASMs caused a great increase in •O and malondialdehyde (MDA) level of the algal cells which indicated the increase in lipid peroxidation of M. aeruginosa. Irreversible membrane damage induced by ASMs via the oxidation of ROS may be an important factor responsible for the algicidal mechanism of ASMs on M. aeruginosa cells. The application of ASMs might provide a new direction to control M. aeruginosa, especially before the exponential phase according to the optimal economy and inhibition effect. Graphical abstract.