Microcystis aeruginosa co-exposure to bisphenol AF and perfluorooctanoic acid promotes cell division and increases microcystin and nitrous oxide emissions

The global rise in cyanobacterial blooms risk parallels the frequent detection of endocrine-disrupting compounds (EDCs) in freshwater, raising the unexplored possibility that EDCs may covertly trigger and sustain these events. This study investigated how bisphenol AF (BPAF) and perfluorooctanoic acid (PFOA) modulated the physiology of Microcystis aeruginosa under different exposure concentrations and sequences. Single-cell transcriptomic and proteomic analyses revealed that low-level co-exposure (0.5 μM) to these chemicals enhanced cell division by 28.99 % via FtsZ upregulation and increased microcystin release by 20.11 %, accompanied by elevated tryptophan- and tyrosine-like fluorescence peaks. High-concentration exposure (5 μM) induced oxidative stress, disrupted cell division, and triggered cell enlargement and secretion of dissolved organic matters. BPAF stimulated nitrous oxide (N₂O) production to 885.11 ng/(10 6 cells·h), whereas PFOA suppressed emissions, compared to 8.93 ng/(10 6 cells·h) in the control group. The nitrogen regulator NtcA was identified as a central node linking nitrogen metabolism, oxidative stress and photosynthetic redox reactions with N₂O synthesis. Molecular docking supported stable interactions between NtcA and both compounds. These findings uncovered distinct regulatory strategies in Microcystis aeruginosa under chemical stress, offering mechanistic insights into how endocrine-disrupting pollutants reshape microbial growth and greenhouse gas emissions in aquatic ecosystems.