Effect of the Antibiotic Norfloxacin on Volatile Organic Compound Emissions From the Cyanobacteria Microcystis aeruginosa

Cyanobacterial volatile organic compounds (VOCs) play important roles in aquatic ecosystems and toxicology. To uncover the promoting mechanisms of norfloxacin on cyanobacterial VOC emissions, the cell growth, reactive oxygen species (ROS) content, photosynthetic performance, and VOC emissions in Microcystis aeruginosa were investigated upon exposure to 10, 30, and 60 μM norfloxacin, and related gene expression was analyzed under the concentration (60 μM) with maximum promotion on the emission. Norfloxacin inhibited cell growth by reducing photosynthetic performance, causing ROS accumulation, and altering normal metabolic processes by changing related gene expression. Seven main compound types were found in M. aeruginosa VOCs, mainly including alcohols, sulfocompounds, benzenes, aldehydes, terpenoids, hydrocarbons, and esters. For almost all VOC components (except β-cyclocitral), norfloxacin promoted their emission by up-regulating related genes, including seven genes in sulfocompound biosynthesis, seven genes in benzene biosynthesis, four genes in terpene biosynthesis, and four genes in fatty acid derivative (aldehydes, alcohols, hydrocarbons, and esters) formation. For β-cyclocitral, its increased emission under norfloxacin stress might result from the accumulated ROS rupturing the C7C8 double bonds of β-carotene. These findings demonstrated that antibiotics could improve VOC emissions from cyanobacteria by up-regulating related genes and increasing ROS accumulation (only for β-cyclocitral), which might intensify water odor, promote cyanobacteria dominating eutrophicated waters, and facilitate atmospheric chemical reactions above the waters.