The potential accumulation of chlorinated organophosphorus flame retardants (Cl-OPFRs) in aquatic environments sparked interest in studying the effects of Cl-OPFRs on cyanobacterial blooms. In this work, two common Cl-OPFRs, tris(1,3-dichloro-2-propyl) phosphate (TDCPP) and tris(2-chloroethyl) phosphate (TCEP), induced dose-dependent biphasic effect on bloom-forming M. aeruginosa. The hormetic response to low-dose Cl-OPFRs was associated with the upregulation of the type I NADH dehydrogenase (NDH-1) complex and its mediated cyclic electron transfer (CET) pathway, as reflected by a transient post-illumination increase in chlorophyll fluorescence, the dark reduction of P700+ and the change of NDH-1-related gene expression. The increased CET activity and carotenoid content jointly reduced the intracellular ROS production, facilitating cyanobacterial growth. Conversely, a higher concentration of both Cl-OPFRs induced severe inhibition of growth and photosynthetic oxygen-evolving activity through an imbalance between PSII and PSI. Toxic-dose Cl-OPFRs inhibited state transition and fixed cells into the State I with a higher PSII/PSI ratio, as indicated by chlorophyll fluorescence induction, 77 K fluorescence emission spectra and photosystem stoichiometry. The elevated PSII/PSI ratio created an imbalance between the two photosystems and eventually lead to ROS overproduction, which generate adverse effects on cell growth. This work provides important insights into the hormetic mechanism of Cl-OPFRs on Microcystis aeruginosa and their potential roles in harmful cyanobacteria blooms.
Keywords: Chlorinated organophosphorus flame retardants; Hormesis; Microcystis aeruginosa; Photosynthesis; ROS.
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