Suppression of water-bloom cyanobacterium Microcystis aeruginosa by algaecide hydrogen peroxide maximized through programmed cell death

Tingru Zhou, Huansheng Cao, Jie Zheng, Fei Teng, Xuejian Wang, Kai Lou, Xihui Zhang, Yi Tao

Research output: Contribution to journalArticle


The global expansion and intensification of toxic cyanobacterial blooms require effective algaecides. Algaecides should be selective, effective, fast-acting, and ideally suppress cyanotoxin production. In this study, whether both maximum growth suppression and minimal toxin production can be simultaneously achieved was tested with a selective algaecide H2O2, through its ability to induce apoptosis-like programmed cell death (AL PCD) in a common bloom species Microcystis aeruginosa. Under doses of 1−15 mg L−1, non-monotonic dose-response suppression of H2O2 on M. aeruginosa were observed, where maximal cell death and minimal microcystin production both occurred at a moderate dose of 10 mg L−1 H2O2. Maximal cell death was indeed achieved through AL PCD, as revealed by integrated biochemical, structural, physiological and transcriptional evidence; transcriptional profile suggested AL PCD was mediated by mazEF and lexA systems. Higher H2O2 doses directly led to necrosis in M. aeruginosa, while lower doses only caused recoverable stress. The integrated data showed the choice between the two modes of cell death is determined by the intracellular energy state under stress. A model was proposed for suppressing M. aeruginosa with AL PCD or necrosis. H2O2 was demonstrated to simultaneously maximize the suppression of both growth and microcystin production through triggering AL PCD.

Original languageEnglish (US)
Article number122394
JournalJournal of Hazardous Materials
StatePublished - Jul 5 2020



  • Apoptosis-like programmed cell death
  • Hydrogen peroxide
  • microcysin-LR
  • Microcystis
  • Non-monotonic dose-response
  • Transcriptome

ASJC Scopus subject areas

  • Environmental Engineering
  • Environmental Chemistry
  • Waste Management and Disposal
  • Pollution
  • Health, Toxicology and Mutagenesis

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