Addressing the threat of harmful cyanobacterial blooms (CyanoHABs) and their associated microcystins (MCs) is crucial for global drinking water safety. In this review, we comprehensively analyze and compares the physical, chemical, and biological methods and genetic engineering for MCs degradation in aquatic environments. Physical methods, such as UV treatments and photocatalytic reactions, have a high efficiency in breaking down MCs, with the potential for further enhancement in performance and reduction of hazardous byproducts. Chemical treatments using chlorine dioxide and potassium permanganate can reduce MC levels but require careful dosage management to avoid toxic by-products and protect aquatic ecosystems. Biological methods, including microbial degradation and phytoremediation techniques, show promise for the biodegradation of MCs, offering reduced environmental impact and increased sustainability. Genetic engineering, such as immobilization of microcystinase A (MlrA) in Escherichia coli and its expression in Synechocystis sp., has proven effective in decomposing MCs such as MC-LR. However, challenges related to specific environmental conditions such as temperature variations, pH levels, presence of other contaminants, nutrient availability, oxygen levels, and light exposure, as well as scalability of biological systems, necessitate further exploration. We provide a comprehensive evaluation of MCs degradation techniques, delving into their practicality, assessing the environmental impacts, and scrutinizing their efficiency to offer crucial insights into the multifaceted nature of these methods in various environmental contexts. The integration of various methodologies to enhance degradation efficiency is vital in the field of water safety, underscoring the need for ongoing innovation.

Cyanobacteria blooms (CBs) caused by eutrophication pose a global concern, especially Microcystis aeruginosa (M. aeruginosa), which could release harmful microcystins (MCs). The impact of microplastics (MPs) on allelopathy in freshwater environments is not well understood. This study examined the joint effect of adding polystyrene (PS-MPs) as representative MPs and two concentrations (2 and 8 mg/L) of pyrogallol (PYR) on the allelopathy of M. aeruginosa. The results showed that the addition of PS-MPs intensified the inhibitory effect of 8 mg/L PYR on the growth and photosynthesis of M. aeruginosa. After a 7-day incubation period, the cell density decreased to 69.7 %, and the chl-a content decreased to 48 % compared to the condition without PS-MPs (p < 0.05). Although the growth and photosynthesis of toxic Microcystis decreased with the addition of PS-MPs, the addition of PS-MPs significantly resulted in a 3.49-fold increase in intracellular MCs and a 1.10-fold increase in extracellular MCs (p < 0.05). Additionally, the emission rates of greenhouse gases (GHGs) (carbon dioxide, nitrous oxide and methane) increased by 2.66, 2.23 and 2.17-fold, respectively (p < 0.05). In addition, transcriptomic analysis showed that the addition of PS-MPs led to the dysregulation of gene expression related to DNA synthesis, membrane function, enzyme activity, stimulus detection, MCs release and GHGs emissions in M. aeruginosa. PYR and PS-MPs triggered ROS-induced membrane damage and disrupted photosynthesis in algae, leading to increased MCs and GHG emissions. PS-MPs accumulation exacerbated this issue by impeding light absorption and membrane function, further heightening the release of MCs and GHGs emissions. Therefore, PS-MPs exhibited a synergistic effect with PYR in inhibiting the growth and photosynthesis of M. aeruginosa, resulting in additional risks such as MCs release and GHGs emissions. These results provide valuable insights for the ecological risk assessment and control of algae bloom in freshwater ecosystems.

The bloom-forming species Microcystis wesenbergii and M. aeruginosa occur in many lakes globally, and may exhibit alternating blooms both spatially and temporally. As environmental changes increase, cyanobacteria bloom in more and more lakes and are often dominated by M. wesenbergii. The adverse impact of M. aeruginosa on co-existing organisms including zooplanktonic species has been well-studied, whereas studies of M. wesenbergii are limited. To compare effects of these two species on zooplankton, we explored effects of exudates from different strains of microcystin-producing M. aeruginosa (Ma905 and Ma526) and non-microcystin-producing M. wesenbergii (Mw908 and Mw929), on reproduction by the model zooplankter Daphnia magna in both chronic and acute exposure experiments. Specifically, we tested physiological, biochemical, molecular and transcriptomic characteristics of D. magna exposed to Microcystis exudates. We observed that body length and egg and offspring number of the daphnid increased in all treatments. Among the four strains tested, Ma526 enhanced the size of the first brood, as well as total egg and offspring number. Microcystis exudates stimulated expression of specific genes that induced ecdysone, juvenile hormone, triacylglycerol and vitellogenin biosynthesis, which, in turn, enhanced egg and offspring production of D. magna. Even though all strains of Microcystis affected growth and reproduction, large numbers of downregulated genes involving many essential pathways indicated that the Ma905 strain might contemporaneously induce damage in D. magna. Our study highlights the necessity of including M. wesenbergii into the ecological risk evaluation of cyanobacteria blooms, and emphasizes that consequences to zooplankton may not be clear-cut when assessments are based upon production of microcystins alone.

The occurrence of poisoning incidents caused by cyanobacterial blooms has aroused wide public concern. Microcystin-leucine arginine (MC-LR) is a well-established toxin produced by cyanobacterial blooms, which is widely distributed in eutrophic waters. MC-LR is not only hazardous to the water environment but also exerts multiple toxic effects including liver toxicity in both humans and animals. However, the underlying mechanisms of MC-LR-induced liver toxicity are unclear. Herein, we used advanced single-cell RNA sequencing technology to characterize MC-LR-induced liver injury in mice. We established the first single-cell atlas of mouse livers in response to MC-LR. Our results showed that the differentially expressed genes and pathways in diverse cell types of liver tissues of mice treated with MC-LR are highly heterogeneous. Deep analysis showed that MC-LR induced an increase in a subpopulation of hepatocytes that highly express Gstm3, which potentially contributed to hepatocyte apoptosis in response to MC-LR. Moreover, MC-LR increased the proportion and multiple subtypes of Kupffer cells with M1 phenotypes and highly expressed proinflammatory genes. Furthermore, the MC-LR increased several subtypes of CD8+ T cells with highly expressed multiple cytokines and chemokines. Overall, apart from directly inducing hepatocytes apoptosis, MC-LR activated proinflammatory Kupffer cell and CD8+ T cells, and their interaction may constitute a hostile microenvironment that contributes to liver injury. Our findings not only present novel insight into underlying molecular mechanisms but also provide a valuable resource and foundation for additional discovery of MC-LR-induced liver toxicity.

Cyanobacterial harmful algal blooms (cHABs) are pervasive sources of stress resulting in neurotoxicity in fish. A member of the widely distributed Microcystis genus of bloom-forming cyanobacteria, Microcystis wesenbergii can be found in many freshwater lakes, including Dianchi Lake (China), where it has become one of the dominant contributors to the lake\'s recurrent blooms. However, unlike its more well-known counterpart M. aeruginosa, the effects of dense non-microcystin-containing M. wesenbergii blooms are seldom studied. The disturbance of appetite regulation and feeding behaviour can have downstream effects on the growth of teleost fish, posing a significant challenge to aquaculture and conservation efforts. Here we examined the effects of M. wesenbergii blooms on the food intake of Acrossocheilus yunnanensis, a native cyprinid in southern China. This fish species has disappeared in Dianchi Lake, and its reintroduction might be negatively affected by the presence of this newly-dominant Microcystis species. We co-cultured juvenile A. yunnanensis with a non-microcystin-producing strain of M. wesenbergii at initial densities between 5 × 104 and 1 × 106 cells/mL and monitored fish feeding behaviour and changes in neurotransmitter and hormone protein levels. High-density M. wesenbergii cultures increased the feeding rate of co-cultured fish, elevating concentrations of appetite-stimulating signalling molecules (Agouti-related protein and γ-aminobutyric acid), while decreasing inhibitory ones (POMC). These changes coincided with histopathological alterations and reduced somatic indices in brain and intestinal tissues. Given this potential for detrimental effects and dysregulation of food intake, further studies are necessary to determine the impacts of chronic exposure of M. wesenbergii in wild fish.

Ecological risk of micro/nano-plastics (MPs/NPs) has become an important environmental issue. Microcystin-leucine-arginine (MC-LR) produced by Microcystis aeruginosa (M. aeruginosa) is the most common and toxic secondary metabolites (SM). However, the influencing mechanism of MPs and NPs exposure on MC-LR synthesis and release have still not been clearly evaluated. In this work, under both acute (4d) and long-term exposure (10d), only high-concentration (10 mg/L) exposure of amino-modified polystyrene NPs (PS-NH2-NPs) promoted MC-LR synthesis (32.94 % and 42.42 %) and release (27.35 % and 31.52 %), respectively. Mechanistically, PS-NH2-NPs inhibited algae cell density, interrupted pigment synthesis, weakened photosynthesis efficiency, and induced oxidative stress, with subsequent enhancing the MC-LR synthesis. Additionally, PS-NH2-NPs exposure up-regulated MC-LR synthesis pathway genes (mcyA, mcyB, mcyD, and mcyG) combined with significantly increased metabolomics (Leucine and Arginine), thereby enhancing MC-LR synthesis. PS-NH2-NPs exposure enhanced the MC-LR release from M. aeruginosa via up-regulated MC-LR transport pathway genes (mcyH) and the shrinkage of plasma membrane. Our results provide new insights into the long-time coexistence of NPs with algae in freshwater systems might pose a potential threat to aquatic environments and human health.

Microcystins (MCs) and nitrites are coexisted in the environment and have reproductive toxicity. The combined toxic effect and mechanism of MCs and nitrite on spermatogenesis remain largely unclear. In the present study, co-exposure to microcystin-leucine arginine (MC-LR) and sodium nitrite (NaNO2) aggravated testicular damage of Balb/c mice and mitochondrial impairment of spermatogonia, Sertoli cells, and sperm. Furthermore, MC-LR and NaNO2 reduced sperm density with a synergistic effect. In addition, MC-LR and NaNO2 synergistically induced oxidative stress in the reproductive system by decreasing superoxide dismutase (SOD) activity and glutathione (GSH) levels and increasing levels of mitochondrial reactive oxygen species (mtROS) and reactive oxygen species (ROS). More importantly, mitoquidone mesylate (MitoQ), an inhibitor of mtROS, blocked MC-LR and NaNO2-induced spermatogonia and Sertoli cell apoptosis by inhibiting high expression of Bax, Fadd, Caspase-8, and cleaved-Caspase-3. On the other hand, MitoQ suppressed pyroptosis of Sertoli cells by inhibiting the expression of NLRP3, N-GSDMD, and cleaved-Caspase-1. Additionally, MitoQ alleviated co-exposure-induced sperm density reduction and organ index disorders in F1 generation mice. Together, co-exposure of MC-LR and NaNO2 can enhance spermatogenic disorders by mitochondrial oxidative impairment-mediated germ cell death. This study emphasizes the potential risks of MC-LR and NaNO2 on reproduction in realistic environments and highlights new insights into the cause and treatment of spermatogenic disorders.

Microcystis, a type of cyanobacteria known for producing microcystins (MCs), is experiencing a global increase in blooms. They have been recently recognized as potential contributors to the widespread of antibiotic resistance genes (ARGs). By reviewing approximately 150 pieces of recent studies, a hypothesis has been formulated suggesting that significant fluctuations in MCs concentrations and microbial community structure during Microcystis blooms could influence the dynamics of waterborne ARGs. Among all MCs, microcystin-LR (MC-LR) is the most widely distributed worldwide, notably abundant in reservoirs during summer. MCs inhibit protein phosphatases or increase reactive oxygen species (ROS), inducing oxidative stresses, enhancing membrane permeability, and causing DNA damage. This further enhances selective pressures and horizontal gene transfer (HGT) chances of ARGs. The mechanisms by which Microcystis regulates ARG dissemination have been systematically organized for the first time, focusing on the secretion of MCs and the alterations of bacterial community structure. However, several knowledge gaps remain, particularly concerning how MCs interfere with the electron transport chain and how Microcystis facilitates HGT of ARGs. Concurrently, the predominance of Microcystis forming the algal microbial aggregates is considered a hotspot for preserving and transferring ARGs. Yet, Microcystis can deplete the nutrients from other taxa within these aggregates, thereby reducing the density of ARG-carrying bacteria. Therefore, further studies are needed to explore the \'symbiotic - competitive\' relationships between Microcystis and ARG-hosting bacteria under varied nutrient conditions. Addressing these knowledge gaps is crucial to understand the impacts of the algal aggregates on dynamics of waterborne antibiotic resistome, and underscores the need for effective control of Microcystis to curb the spread of antibiotic resistance. Constructed wetlands and photocatalysis represent advantageous strategies for halting the spread of ARGs from the perspective of Microcystis blooms, as they can effectively control Microcystis and MCs while maintaining the stability of aquatic ecosystem.

Surfactant pollution is escalatitheng in eutrophic waters, but the effect of surfactant charge properties on the physiological and biochemical properties of toxin-producing microalgae remains inadequately explored. To address this gap, this study explores the effects and mechanisms of three common surfactants-cetyltrimethylammonium bromide (CTAB, cationic), sodium dodecyl sulfate (SDS, anionic), and Triton X-100 (nonionic)-found in surface waters, on the agglomeration behavior, physiological indicators, and Microcystin-LR (MC-LR) release of Microcystis aeruginosa (M. aeruginosa) by using UV-visible spectroscope, Malvern Zetasizer, fluorescence spectrometer, etc. Results suggest that charge properties significantly affect cyanobacterial aggregation and cellular metabolism. The CTAB-treated group demonstrates a ∼5.74 and ∼9.74 times higher aggregation effect compared to Triton X-100 and SDS (300 mg/L for 180 min) due to strong electrostatic attraction. Triton X-100 outperforms CTAB and SDS in polysaccharide extraction, attributed to its higher water solubility and lower critical micelle concentration. CTAB stimulates cyanobacteria to secrete proteins, xanthohumic acid, and humic acids to maintain normal physiological cells. Additionally, the results of SEM and ion content showed that CTAB damages the cell membrane, resulting in a ∼90% increase in the release of intracellular MC-LR without cell disintegration. Ionic analyses confirm that all three surfactants alter cell membrane permeability and disrupt ionic metabolic pathways in microalgae. This study highlights the relationship between the surface charge properties of typical surfactants and the dispersion/agglomeration behavior of cyanobacteria. It provides insights into the impact mechanism of exogenous surfactants on toxic algae production in eutrophic water bodies, offering theoretical references for managing surfactant pollution and treating algae blooms.

Microcystins (MCs), toxins generated by cyanobacteria, feature microcystin-LR (MC-LR) as one of the most prevalent and toxic variants in aquatic environments. MC-LR not only causes environmental problems but also presents a substantial risk to human health. This study aimed to investigate the impact of MC-LR on APCmin/+ mice, considered as an ideal animal model for intestinal tumors. We administered 40 µg/kg MC-LR to mice by gavage for 8 weeks, followed by histopathological examination, microbial diversity and metabolomics analysis. The mice exposed to MC-LR exhibited a significant promotion in colorectal cancer progression and impaired intestinal barrier function in the APCmin/+ mice compared with the control. Gut microbial dysbiosis was observed in the MC-LR-exposed mice, manifesting a notable alteration in the structure of the gut microbiota. This included the enrichment of Marvinbryantia, Gordonibacter and Family_XIII_AD3011_group and reductions in Faecalibaculum and Lachnoclostridium. Metabolomics analysis revealed increased bile acid (BA) metabolites in the intestinal contents of the mice exposed to MC-LR, particularly taurocholic acid (TCA), alpha-muricholic acid (α-MCA), 3-dehydrocholic acid (3-DHCA), 7-ketodeoxycholic acid (7-KDCA) and 12-ketodeoxycholic acid (12-KDCA). Moreover, we found that Marvinbryantia and Family_XIII_AD3011_group showed the strongest positive correlation with taurocholic acid (TCA) in the mice exposed to MC-LR. These findings provide new insights into the roles and mechanisms of MC-LR in susceptible populations, providing a basis for guiding values of MC-LR in drinking water.