Characterization of a Novel Artemisinin Algicidal Particle and Its Inhibitory Effect on Microcystis aeruginosa.

A new artemisinin sustained-release particle (ASP) was developed that significantly inhibits Microcystis aeruginosa (M. aeruginosa) growth. The physical and chemical properties of ASPs were characterized using scanning electron microscopy (SEM), Fourier transform infrared spectroscopy (FT-IR), X-ray diffraction (XRD), differential scanning calorimetry, and thermogravimetry (DSC-TG). The results demonstrated that ASPs are thermally stable and have sustained-release properties. On the sixth day, the ASPs (0.2 g L-1) inhibited M. aeruginosa with an inhibition rate (IR) greater than 70%. Additionally, ASPs inhibited M. aeruginosa without increasing microcystin-LR release (MC-LR). This research offers a novel approach to the management of cyanobacterial blooms.

An innovative strategy to control Microcystis growth using tea polyphenols sustained-release particles: preparation, characterization, and inhibition mechanism.

Allelochemicals have been shown to inhibit cyanobacterial blooms for several years. In view of the disadvantages of "direct-added" mode, natural and pollution-free tea polyphenolic allelochemicals with good inhibitory effect on cyanobacteria were selected to prepare sustained-release particles by microcapsule technology. Results showed that the encapsulation efficiency of tea polyphenols sustained-release particles (TPSPs) was 50.6% and the particle size ranged from 700 to 970 nm, which reached the nanoscale under optimum preparation condition. Physical and chemical properties of TPSPs were characterized to prove that tea polyphenols were well encapsulated and the particles had good thermal stability. The optimal dosage of TPSPs was determined to be 0.3 g/L, at which the inhibition rate on Microcystis aeruginosa in logarithmic growth period could be maintained above 95%. Simultaneous decrease in algal density and chlorophyll-a content indicated that the photosynthesis of algal cells was affected leading to cell death. Significant changes of antioxidant enzyme activities suggested that Microcystis aeruginosa's antioxidant systems had been disrupted. Furthermore, TPSPs increased the concentration of O2- which led to lipid peroxidation of cell membrane and a subsequent increase in malondialdehyde (MDA) content. Meanwhile, the protein content, nucleic acid content, and electrical conductivity in culture medium rose significantly indicating the cell membrane was irreversibly damaged. This work can provide a basis for the utilization of environmentally friendly algal suppressants.

Integrated transcriptomic and metabolomic analysis of Microcystis aeruginosa exposed to artemisinin sustained-release microspheres.

Artemisinin sustained-release microspheres (ASMs) have been shown to inhibit Microcystis aeruginosa (M. aeruginosa) blooms. Previous studies have focused on inhibitory mechanism of ASMs on the physiological level of M. aeruginosa, but the algal inhibitory mechanism of ASMs has not been comprehensively and profoundly revealed. The study proposed to reveal the toxicity mechanism of ASMs on M. aeruginosa based on transcriptomics and metabolomics. After exposure to 0.2 g·L-1 ASMs for 7 days, M. aeruginosa biomass was significantly inhibited, with an inhibition rate (IR) of 47 % on day 7. Transcriptomic and metabolomic results showed that: (1) 478 differentially expressed genes (DEGs) and 251 differential metabolites (DMs) were obtained; (2) ASMs inhibited photosynthesis by blocking photosynthetic pigment synthesis, destroying photoreaction centers and photosynthetic carbon reactions; (3) ASMs reduced L-glutamic acid content and blocked glutathione (GSH) synthesis, leading to an imbalance in the antioxidant system; (4) ASM disrupted nitrogen metabolism and the hindered synthesis of various amino acids; (5) ASMs inhibited glyoxylate cycle and TCA cycle. This study provides an important prerequisite for the practical application of ASMs and a new perspective for the management of harmful algal blooms (HABs).