6PPD-quinone affects the photosynthetic carbon fixation in cyanobacteria by extracting photosynthetic electrons.

Photosynthetic carbon fixation by cyanobacteria plays a pivotal role in the global carbon cycle but is threatened by environmental pollutants. To date, the impact of quinones, with electron shuttling properties, on cyanobacterial photosynthesis is unknown. Here, we present the first study investigating the effects of an emerging quinone pollutant, i.e., 6PPD-Q (N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone), on the cyanobacterium Synechocystis sp. over a 400-generation exposure period. Synechocystis sp. exhibited distinct sequential phases, including hormesis, toxicity, and eventual recovery, throughout this exposure. Extensive evidence, including results of thylakoid membrane morphological and photosynthetic responses, carbon fixation rate, and key gene/protein analyses, strongly indicates that 6PPD-Q is a potent disruptor of photosynthesis. 6PPD-Q accepts photosynthetic electrons at the plastoquinone QB site in photosystem II (PSII) and the phylloquinone A1 site in PSI, leading to a sustained decrease in the carbon fixation of cyanobacteria after an ephemeral increase. This work revealed the specific mechanism by which 6PPD-Q interferes with photosynthetic carbon fixation in cyanobacteria, which is highly important for the global carbon cycle.

Differential toxicity of various mineral nanoparticles to Synechocystis sp.: With and without ciprofloxacin.

Mineral nanoparticles (M-NPs) are ubiquitous in aquatic environments, but their potential harms to primary producers and impacts on the toxicity of coexisting pollutants are largely unknown. Herein, the toxicity mechanisms of various M-NPs (i.e., SiO2, Fe2O3, Al2O3, and TiO2 NPs) to Synechocystis sp. in absence and presence of ciprofloxacin (CIP) were comprehensively investigated. The heteroaggregation of cells and M-NPs can hinder substrate transfer or light acquisition. The attraction between Synechocystis sp. and M-NPs increased in the order of SiO2 < Fe2O3 < Al2O3 ≈ TiO2 NPs. Therefore, SiO2 and Fe2O3 NPs exerted slight effects on physiology and proteome of Synechocystis sp.. Al2O3 NPs with the rod-like shape caused physical damage to cells. Differently, TiO2 NPs with photocatalytic activities provided photogenerated electrons for Synechocystis sp., promoting photosynthesis and the Calvin cycle for CO2 fixation. SiO2, Fe2O3, and Al2O3 NPs alleviated the toxicity of CIP in an adsorption-depended manner. Conversely, the combination of CIP and TiO2 NPs exerted more pronounced toxic effects compared to their individuals, and CIP disturbed the extracellular electron transfer from TiO2 NPs to cells. The findings highlight the different effects of TiO2 NPs from other M-NPs on cyanobacteria, either alone or in combination with CIP, and improve the understanding of toxic mechanisms of M-NPs.

Black carbon and humic acid alleviate the toxicity of antibiotics to a cyanobacterium Synechocystis sp.

Natural organic matters (NOMs), omnipresent in natural water, challenge the toxicity assessment of pollutants to aquatic organisms due to their complex interactions with chemicals and organisms. Here, we investigated the combined toxicity of one solid NOM (black carbon, BC) or one soluble NOM (humic acid, HA) with antibiotics, roxithromycin (RTM) or gatifloxacin (GAT), to the cyanobacterium Synechocystis sp.. The NOMs alleviated the toxicity of RTM and GAT to Synechocystis sp., and BC had greater alleviation effects than HA due to its stronger adsorption to antibiotics. Antibiotics disturbed the photosynthesis of Synechocystis sp. significantly, which were also mitigated by BC and HA. Proteomic analysis showed that BC up-regulated the pathway of ribosome and photosynthetic antenna protein. GAT down-regulated the pathways of ABC transporter and oxidative phosphorylation. RTM interfered the pathway of porphyrin and chlorophyll metabolism. Furthermore, the addition of BC reduced the number of differentially expressed proteins caused by antibiotics, corroborating its mitigation effects on the toxicity of antibiotics. The disturbance of HA on the pathway of ABC transporters inhibited the internalization of RTM, thus decreasing its toxicity. This study underscores the significance of NOMs in mediating the toxicity of organic pollutants to aquatic organisms in natural waters.

Single and combined genotoxicity of metals and fluoroquinolones to zebrafish embryos at environmentally relevant concentrations.

Fluoroquinolones (FQs) are known to have genotoxicity to aquatic organisms. However, their genotoxicity mechanisms, individually and in combination with heavy metals, are poorly understood. Here, we investigated the single and joint genotoxicity of FQs, ciprofloxacin (CIP) and enrofloxacin (ENR), and metals (Cd and Cu) at environmentally relevant concentrations (0.2 µM) to zebrafish embryos. We found that FQs or/and metals induced genotoxicity (i.e., DNA damage and cell apoptosis) to zebrafish embryos. Compared with their single exposure, the combined exposure of FQs and metals elicited less ROS overproduction but higher genotoxicity, suggesting other toxicity mechanisms may also act in addition to oxidation stress. The upregulation of nucleic acid metabolites and the dysregulation of proteins confirmed the occurrence of DNA damage and apoptosis, and further revealed the inhibition of DNA repair by Cd and binding of DNA or DNA topoisomerase by FQs. This study deepens the knowledge on the responses of zebrafish embryos to exposure of multiple pollutants, and highlights the genotoxicity of FQs and heavy metals to aquatic organisms.

Interactions between antibiotics and heavy metals determine their combined toxicity to Synechocystis sp.

Co-pollution of antibiotics and metals is prevailing in aquatic environments. However, risks of coexisted antibiotics and metals on aquatic organisms is unclear. This study investigated the combined toxicity of antibiotics and metals towards Synechocystis sp. PCC 6803, a cyanobacterium. We found that the joint toxicity of antibiotics and metals is dependent on their interplays. The complexation between chlortetracycline (CTC) and copper/cadmium (Cu(II)/Cd(II)) resulted in their antagonistic toxicity. Contrarily, an additive toxicity was found between florfenicol (FLO) and Cu(II)/Cd(II) due to lack of interactions between them. CTC facilitated the intracellular uptake of Cu(II) and Cd(II) by increasing the membrane permeability. However, FLO had no obvious effects on the internalization of metals in Synechocystis sp. Proteomic analysis revealed that the photosynthetic proteins was down-regulated by CTC and FLO, and ribosome was the primary target of FLO. These results were verified by parallel reaction monitoring (PRM). Cu(II) induced the up-regulation of iron-sulfur assembly, while Cd(II) disturbed the cyclic electron transport in Synechocystis sp. The co-exposure of CTC and metals markedly alleviated the dysregulation of proteins, while the co-exposure of FLO and metals down-regulated biological functions such as ATP synthesis, photosynthesis, and carbon fixation of Synechocystis sp., compared with their individuals. This supports their joint toxicity effects. Our findings provide better understanding of combined toxicity between multiple pollutants in aquatic environments.

Pollutants affect algae-bacteria interactions: A critical review.

With increasing concerns on the ecological risks of pollutants, many efforts have been devoted to revealing the toxic effects of pollutants on algae or bacteria in their monocultures. However, how pollutants affect algae and bacteria in their cocultures is still elusive but crucial due to its more environmental relevance. The present review outlines the interactions between algae and bacteria, reveals the influential mechanisms of pollutants (including pesticides, metals, engineered nanomaterials, pharmaceutical and personal care products, and aromatic pollutants) to algae and bacteria in their coexisted systems, and puts forward prospects for further advancing toxic studies in algal-bacterial systems. Pollutants affect the physiological and ecological functions of bacteria and algae by interfering with their relationships. Cell-to-cell adhesion, substrate exchange and biodegradation of organic pollutants, enhancement of signal transduction, and horizontal transfer of tolerance genes are important defense strategies in algal-bacterial systems to cope with pollution stress. Developing suitable algal-bacterial models, identifying cross-kingdom signaling molecules, and deciphering the horizontal transfer of pollutant resistant genes between algae and bacteria under pollution stress are the way forward to fully exploit the risks of pollutants in natural aquatic environments.

Unraveling individual and combined toxicity of nano/microplastics and ciprofloxacin to Synechocystis sp. at the cellular and molecular levels.

Although nanoplastics/microplastics (NPs/MPs) may interact with co-contaminants (e.g. antibiotics) in aquatic systems, little is known about their combined toxicity. Here, we compared the individual toxicity of NPs/MPs or ciprofloxacin (CIP, a very commonly detected antibiotic) and their combined toxicity toward a unicellular cyanobacterium Synechocystis sp. in terms of the cellular responses and metabolomic analysis. We found that CIP exhibited an antagonistic effect with NPs/MPs due to its adsorption onto the surface of NPs/MPs. Particle size-dependent toxic effects of NPs/MPs were observed. Reactive oxygen species (ROS) was verified as an important factor for NPs/MPs to inhibit cell growth, other than for CIP. Metabolomics further revealed that Synechocystis sp. up-regulated glycerophospholipids, amino acids, nucleotides, and carbohydrates to tolerate CIP pressure. NPs/MPs downregulated the TCA cycle and glycerophospholipids metabolism and impaired the primary production and membrane integrity via adhesion with Synechocystis sp.. Additionally, the toxicity of NPs/MPs throughout ten growth cycles at a sublethal concentration unveiled its potential risks in interfering with metabolism. Collectively, our findings provide insights into the joint ecotoxicity of NPs/MPs and antibiotics, and highlight the potential risks of co-pollutants at environmental relevant concentrations.