Growth suppression and apoptosis-like cell death in Microcystis aeruginosa by H2O2: A new insight into extracellular and intracellular damage pathways.

Published

Journal Article

H2O2 has been suggested and applied as effective algaecide for harmful cyanobacterial bloom control, however, the transport of exogenous H2O2 into microalgal cells, the subsequent intracellular damage pathway and dose-response variations were little studied. We addressed these questions in a bloom-forming cyanobacterium Microcystis aeruginosa with H2O2 at 0.1-1.5 mM. The results showed that H2O2 at 0.4 mM and above significantly suppressed M. aeruginosa growth for over two weeks, and induced apoptosis-like death in terms of membrane potential dissipation, caspase-3 activation, chromatin condensation, and lysis induction. However, the dose-response effects were not monotonic. H2O2 at 0.7 mM resulted in the severest growth suppression among 0.1-1.5 mM treatments, including the lowest biomass for 74% loss, the highest cell lysis ratio for 79%, and the highest utilization rate of H2O2 for 0.101 mM d-1. Moreover, several evidence point to severer apoptosis-like cell death in 0.7 mM treatments, involving fastest and severest cell lysis, smallest cell size and wrinkled surface and lowest membrane potential. Therefore, the apoptosis-like cell death induced by H2O2 at moderate dosages should be a crucial cause for the non-monotonic dose-response effects on growth suppression. Additionally, intracellular H2O2 level increased rapidly within 20 min after exposure at 0.4 mM and above, directly confirming the transport of exogenous H2O2 into M. aeruginosa cells and the intracellular damages due to subsequent elevation in intracellular oxidative stress. The study demonstrates that H2O2 at moderate dosages could be a promising method for the biomass control, in a fast and efficient way, on M. aeruginosa blooms.

Full Text

Duke Authors

Cited Authors

  • Zhou, T; Zheng, J; Cao, H; Wang, X; Lou, K; Zhang, X; Tao, Y

Published Date

  • November 2018

Published In

Volume / Issue

  • 211 /

Start / End Page

  • 1098 - 1108

PubMed ID

  • 30223325

Pubmed Central ID

  • 30223325

Electronic International Standard Serial Number (EISSN)

  • 1879-1298

International Standard Serial Number (ISSN)

  • 0045-6535

Digital Object Identifier (DOI)

  • 10.1016/j.chemosphere.2018.08.042

Language

  • eng