Due to the large-scale outbreak of Corona Virus Disease (2019), amounts of disinfecting agents was regularly used in public environments and their potential toxicity towards organisms needed to be appreciated. Thus, one mostly used cationic disinfectant, benzalkonium chlorides (BAC(C12)), was selected to assess its potential toxicity one common cyanobacteria Microcystis aeruginosa (M. aeruginosa) in this study. The aims were to explore the toxic effect and mechanism of BAC (C12) on M. aeruginosa growth within 96 h via morphological, physiological, and the relative and absolute quantification (iTRAQ)-based quantitative proteomics variations. The results found that BAC(C12) significantly inhibited cell density of M. aeruginosa at concentrations from 1 mg/L to 10 mg/L, and the 96-h EC₅₀ value was identified to be 3.61 mg/L. Under EC₅₀ concentration, BAC(C12) depressed the photosynthesis activities of M. aeruginosa exhibited by 36% decline of the maximum quantum yield for primary photochemistry (Fv/Fm) value and denaturation of photosynthetic organelle, caused oxidative stress response displayed by the increase of three indexes including superoxide dismutase (SOD), malondialdehyde (MDA), and the intracellular reactive oxygen species (ROS), and destroyed the integrity of cell membranes demonstrated by TEM images and the increase of ex-cellular substances. Then, the iTRAQ-based proteomic analysis demonstrated that BAC(C12) depressed photosynthesis activities through inhibiting the expressions of photosynthetic protein and photosynthetic electron transport related proteins. The suppression of electron transport also led to the increase of superoxide radicals and then posed oxidative stress on cell. Meantime, the 63.63% ascent of extracellular microcystin production of M. aeruginosa was observed, attributing to the high expression of microcystin synthesis proteins and the damage of cell membrane. In sum, BAC(C12) exposure inhibited the growth of M. aeruginosa mainly by depressing photosynthesis, inducing oxidative stress, and breaking the cell membrane. And, it enhanced the release of microcystin from the cyanobacterial cells via up-regulating the microcystin synthesis proteins and inducing the membrane damage, which could enlarge its toxicity to aquatic species.

Aggravating the pollution of microcystins (MCs) in freshwater environments is detrimental to aquatic living organisms and humans, and thus threatens the stability of ecosystems. Some environmental factors have been verified to promote the production of MCs in Microcystis aeruginosa, thereby aggravating the pollution of MCs. However, the effects of cerium (Ce), the most abundant rare earth element in global water environments, on the production of MCs in M. aeruginosa are unknown. Here, Lake Taihu water was selected as a representative of freshwater environments. By using interdisciplinary methods, it was found that: (1) the exposure level of Ce [Ce(III) and Ce(IV)] in Lake Taihu water is in the range of 0.271–0.282 μg/L; (2) Ce exposure in Lake Taihu water promoted the contents of three main MCs (MC-LR, MC-LW and MC-YR) in M. aeruginosa and water; (3) a cellular mechanism of Ce promoting the production of MCs in M. aeruginosa in Lake Taihu water was suggested: Ce enhanced endocytosis in cells of M. aeruginosa to promote the essential element uptake by M. aeruginosa for MC synthesis. Thus, Ce exposure in Lake Taihu water aggravates the pollution of MCs via enhancing endocytosis in cells of M. aeruginosa. The results provide reference for assessing the environmental risk of Ce in water environments, investigating the mechanism of the pollution of MCs induced by environmental factors, and developing strategies aimed at preventing and controlling the pollution of MCs.

The excessive proliferation of Microcystis aeruginosa can lead to ecological damage, economic losses, and threaten animal and human health. For controlling Microcystis blooms, microorganism-based methods have attracted much attention from researchers because of their eco-friendliness and species-specificity. Herein, we first found that a Paucibacter strain exhibits algicidal activity against M. aeruginosa and microcystin degradation capability. The algicidal activity of DH15 (2.1 × 10⁴ CFU/ml) against M. aeruginosa (2 × 10⁶ cells/ml) was 94.9% within 36 h of exposure. DH15 also degraded microcystin (1.6 mg/L) up to 62.5% after 72 h. We demonstrated that the algicidal activity of DH15 against M. aeruginosa can be mediated by physical attachment and indirect attack: (1) Both washed cells and cell-free supernatant could kill M. aeruginosa efficiently; (2) Treatment with DH15 cell-free supernatants caused oxidative stress, altered the fatty acid profile, and damaged photosynthetic system, carbohydrate, and protein metabolism in M. aeruginosa. The combination of direct and indirect attacks supported that strain DH15 exerts high algicidal activity against M. aeruginosa. The expression of most key genes responsible for photosynthesis, antioxidant activity, microcystin synthesis, and other metabolic pathways in M. aeruginosa was downregulated. Strain DH15, with its microcystin degradation capacity, can overcome the trade-off between controlling Microcystis blooms and increasing microcystin concentration. Our findings suggest that strain DH15 possesses great potential to control outbreaks of Microcystis blooms.

The development of saline-alkali lands has contributed to the increasing discharge of alkaline salt-laden wastewater, which poses a threat to aquatic organisms. However, the comprehensive effect of alkaline salt on Microcystis aeruginosa, a harmful cyanobacterium, remains unclear. In this study, the growth, physiology, cell ultrastructure and production of microcystin-LR (MC-LR) in Microcystis aeruginosa exposed to four levels of alkaline salt stress were evaluated. The growth of Microcystis aeruginosa was stimulated at an electrical conductivity (EC) of 2.5 mS/cm compared to the control, as supported by the increased cell density, photosynthetic pigment and protein contents. Microcystis aeruginosa could tolerate a certain level of alkaline salt (i.e., EC of 5 mS/cm) via increasing photosynthetic pigment contents to protect cells from alkaline salt stress, but the antioxidant defence system and cell ultrastructure were not affected. When EC increased to 7.5 mS/cm, alkaline salt caused oxidative stress and toxicity in Microcystis aeruginosa, as evidenced by analysis of the integrated biomarker response (IBR). Furthermore, the photosynthetic pigment and protein contents decreased, and cell apoptosis associated with ultrastructural changes was observed. Therefore, we propose that EC of 7.5 mS/cm is a threshold for growth of Microcystis aeruginosa. Additionally, the intracellular MC-LR content was stimulated by alkaline salt, and the highest value was observed at EC of 2.5 mS/cm. The extracellular MC-LR content increased with the increasing alkaline salt concentration. When EC was 7.5 mS/cm, the extracellular MC-LR content was significantly higher than in the control and was associated with the upregulated mcyH gene. This study recommends that more attention should be paid to the risk of Microcystis aeruginosa bloom and microcystin-LR pollution in lakes located in salinization regions.

Colony formation is an essential stage of cyanobacterial blooms. High calcium concentration can promote Microcystis aeruginosa aggregation behavior, but the mechanism of colony formation caused by calcium has rarely been reported. In this study, high calcium-induced colony formation was identified as a shift from cell adhesion to cell division, rather than only cell adhesion as previously thought. Algae responded to this calcium-induced environmental pressure by aggregating and forming colonies. Algal cells initially secreted large quantities of extracellular polysaccharides (EPS) and rapidly aggregated by cell adhesion. The highest aggregation proportion was up to 68.93%. However, high calcium concentrations cannot completely inhibit algal cell growth, but only delay the algae into the rapid growth phase. With adaption to calcium and existing high EPS content, the daughter cells reduced EPS synthesis and the aggregation proportion decreased. The increasing growth rate was also responsible for the decreased xylose content in EPS. The mechanism of colony formation changed to cell division. The downregulation of genes related to EPS secretion also supported this hypothesis. Overall, these results can benefit for our understanding of cyanobacterial bloom formation.

In this study, we treated harmful Microcystis aeruginosa cyanobacteria using chitosan-modified nanobubbles. The chitosan-modified nanobubbles (255 ± 19 nm) presented a positive zeta potential (15.36 ± 1.17 mV) and generated significantly (p < 0.05) more hydroxyl radicals than the negatively charged nanobubbles (−20.68 ± 1.11 mV). Therefore, the interaction between the positively charged chitosan-modified nanobubbles and negatively charged M. aeruginosa (−34.81 ± 1.79 mV) was favored. The chitosan-modified nanobubble treatment (2.20 × 10⁸ particles mL⁻¹) inactivated 73.16% ± 2.23% of M. aeruginosa (2.00 × 10⁶ cells mL⁻¹) for 24 h without causing significant cell lysis (≤0.25%) and completely inhibited the acute toxicity of M. aeruginosa toward Daphnia magna. The inactivation was correlated (r² = 0.97) with the formation of reactive oxygen species (ROS) in M. aeruginosa. These findings indicated that the hydroxyl radicals generated by the chitosan-modified nanobubbles disrupted cell membrane integrity and enhanced oxidative stress (ROS formation), thereby inactivating M. aeruginosa. Moreover, the penetration of the chitosan-modified nanobubbles and cell alterations in M. aeruginosa were visually confirmed. Our results suggested that the chitosan-modified nanobubble treatment is an eco-friendly method for controlling harmful algae. However, further studies are required for expanding its practical applications.

Microcystins (MCs) are produced during the growth and proliferation of some species of cyanobacteria, mainly Microcystis aeruginosa, which has massive growth in eutrophic water bodies. Microcystins are highly toxic metabolites derived from some cyanobacteria species that exert its main effect in the liver through the inhibition of protein phosphatase (PP1 and PP2A). However, other damages in fish species are less documented and could be unexpected. The aim of the current study was to evaluate the effects of Microcystis aeruginosa extract (MaE) into the central nervous system (CNS) of the Nile tilapia. The MaE was normalized by MCs content (MC-LR). We include a positive control for protein phosphatase inhibition, norcantharidin intraperitoneally dosed at sublethal levels. On the eighth day, measurement of neurotransmission biomarkers (AChE, BChE, CbE, and GABA) were measured, as well as levels of mitochondrial calcium and the mitochondrial membrane potential by flow cytometry in the brain and spinal cord were assessed, in addition to the PP1/PP2A activity in the liver. The MCs elicited mortality at 5 µg/L. The positive control and MCs at sublethal levels inhibited the PP1/PP2A activity in the liver and induced alterations in the neurotoxicity biomarkers evaluated in the CNS. This response is probably due to the disruption of transport ions, dependent and independent of ATP because of alterations in the mitochondrial membrane potential and mitochondrial calcium. The findings of this study suggest that pollutants capable of inducing cyanobacterial blooms are able, in an indirect way, to exert neurotoxic effects in fish species through MC levels.

Iron oxide nanoparticles (nano-Fe₂O₃) widely distribute in waters with low toxicity to aquatic organisms. But it is unclear for nano-Fe₂O₃ to affect the fate of coexisting arsenic (As) with its bioaccumulation and biotransformation. In this study, we thus mainly investigated arsenate (As(V)) toxicity, uptake kinetics, biotransformation and subcellular distribution in Microcystis aeruginosa influenced by nano-Fe₂O₃. The results showed that M. aeruginosa was more sensitive to As(V) associated with nano-Fe₂O₃. Due to the exaggerated increase of efflux rate constants of As compared with the uptake rate constants in algal cells affected by different levels of nano-Fe₂O₃, the As(V) bioconcentration factor decreased with nano-Fe₂O₃ increasing correspondingly, indicating that As bioaccumulation was diminished by nano-Fe₂O₃. The decreased As accumulation in M. aeruginosa could be supported by the evidential As(V) sequestration through high adsorption of nano-Fe₂O₃, which resulted in decreasing free As level for algae uptake in media. Meanwhile, As subcellular distribution was adjusted by nano-Fe₂O₃ with decreasing in cell walls and rising in cytoplasmic organelles compared with nano-Fe₂O₃ free. As(V) reduction and methylation were enhanced with increasing nano-Fe₂O₃, stimulating by its sensitivity to the interaction of nano-Fe₂O₃ and As(V) as well as the rising level of As in cytoplasmic organelles of this algae. It is confirmed by the higher relative gene expression levels of arsC and arsM in elevated nano-Fe₂O₃. Accordingly, it is highlighted to be deserved more attention that the changing behavior of As(V) by nano-Fe₂O₃ that reduce As bioaccumulation and accelerate its biotransformation in algae in As contaminated water.

In recent years, cyanobacteria blooms have continued to erupt frequently, seriously jeopardizing the safety of drinking water and human health. The safe, quick, and economical removal of cyanobacteria from water bodies, especially the dominant species of cyanobacteria, Microcystis aeruginosa, has captured a lot of scientists’ attention. The application of advanced oxidation technology in water treatment is very promising, but it has not yet been used in production. To further promote the application of the advanced oxidation method in water treatment, this article combines the results of advanced research in China and abroad to review this emergent technology. Briefly, advanced oxidation process methods employ various mechanisms to remove the dominant species of cyanobacteria blooms Microcystis aeruginosa. This provides a theoretical reference and support for the efficient removal of harmful cyanobacteria from water.

Spinetoram is one of the most worldwidely used pesticides for its high insecticidal efficacy and low human toxicity. Following the large usage of spinetoram, the ecotoxicity and environmental risks to aquatic ecosystems have call for urgent study. In the present study, we investigated the combined effects of spinetoram and the harmful alga Microcystis aeruginosa in freshwater, on survival and reproduction of Daphnia pulex. Acute toxicity test of spinetoram resulted in negative effects on survival, with a 48-h LC₅₀ value of 37.71 μg L⁻¹. Under the long-time exposure to environmentally relevant concentrations (0.18 and 0.35 μg L⁻¹) of spinetoram and a low composition of Microcystis (30%) in the diet, D. pulex showed both shorter longevity and lower fecundity; the time to first brood also increased. At population level, carrying capacity was highly decreased by spinetoram and Microcystis, whereas a significant decrease of intrinsic growth rate was observed at 0.35 μg L⁻¹ spinetoram with 30% Microcystis as food. The present study highlighted that pesticide spinetoram had highly toxic effects on D. pulex and could reduce the tolerance of D. pulex to M. aeruginosa, causing great effects on D. pulex population in natural waterbodies.