Moxifloxacin (MOX), a widely used novel antibiotic, may pose ecological risks at its actual environmental concentrations, as has been detected in aquatic systems. However, its ecotoxicity to aquatic organisms and regulatory mechanisms of phosphorus in eutrophic aqueous environments are still limited. This study aimed to analyze its physiological and biochemical parameters, including cellular growth, chlorophyll fluorescence, photosynthetic pigments, oxidative stress biomarkers, and metabolomics to elucidate the toxicity induced by environmental concentrations of MOX inMicrocystis aeruginosaat different phosphorus levels. The results revealed that the EC50values of MOX onM. aeruginosaat different phosphorus concentrations were 8.03, 7.84, and 6.91 μg/L, respectively, indicating MOX toxicity was exacerbated with increasing phosphorus levels. High phosphorus intensified the suppression of chlorophyll fluorescence and photosynthetic pigments, while activating the antioxidant enzyme, indicating severe peroxidation damage. Metabolomic analysis showed MOX induced different discriminating metabolites under different phosphorus levels, and perturbed more biological pathways at higher phosphorus concentrations, such as starch and sucrose metabolism, pyrimidine metabolism, and glycerolipid metabolism. This indicates that phosphorus plays an important role in regulating metabolism inM. aeruginosaexposed to MOX. The findings provide valuable information on the mechanisms involved in cyanobacteria responses to antibiotic stress, and offer a theoretical basis for accurately assessing antibiotic toxicity in eutrophic aqueous environments.
The increasing use of nanoparticles (NPs) has raised concerns about their potential environmental risks. Many researches on NPs focused on the toxicity mechanism to microorganisms , but neglect the toxicity effects in relation to nutritional conditions. Here, we evaluated the interactive effects of zinc oxide (ZnO) NPs and phosphorus (P) levels on the bacterial community and functioning of periphytic biofilms. Results showed that long-term exposure to ZnO NPs significantly reduced alkaline phosphatase activity (APA) of periphytic biofilms just in P-limited conditions. Co-occurrence network analysis indicated that ZnO NPs exposure reduced network complexity between bacterial taxa in P-limited conditions, while the opposite trend was observed in P-replete conditions. Correlation analysis and random forest modeling suggested that excessive Zn 2+ released and high reactive oxygen species (ROS) production might be mainly responsible for the inhibition of APA induced by ZnO NPs under P-limited conditions, while adjustment of bacterial diversity and improvement of keystone taxa cooperation were the main mechanisms in maintaining APA when subjected to weak toxicity of ZnO NPs in P-replete conditions. Taken together, our results provide insights into the biological feedback mechanism involved in ZnO NPs exposure on the ecological function of periphytic biofilms in different P nutritional conditions.
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