Hydrogen peroxide induces apoptotic-like cell death inMicrocystis aeruginosa(Chroococcales, Cyanobacteria) in a dose-dependent manner

Abstract

We investigated the capability of Microcystis aeruginosa to cause apoptosis by pursuing morphological, molecular and physiological characteristics after exposure to H 2 O 2 . Microcystis proliferation was only weakly affected after exposure to 150 mM H 2 O 2 but cell numbers decreased dramatically after exposures of 250 and 325 mM H 2 O 2 . Cells exposed to 250 and 325 mM H 2 O 2 were examined using transmission electron microscopy, and they exhibited membrane deformation and partial disintegration of thylakoids. Correspondingly, fluorescence imaging of DNA by Hoechst 33342 staining revealed the condensation of nucleoid chromatin. Moreover, cellular injury was concomitant with dramatic decreases in photosynthetic efficiency (ratio of variable fluorescence to maximum fluorescence [Fv/Fm], maximum electron transport rate [ETRmax]) and elevated caspase-3-like activity after exposure of 250 and 325 mM H 2 O 2 . Terminal deoxynucleotidyl transferase Deoxyuridine 5-triphosphate nick end labelling (TUNEL) positive staining appeared in cells exposed to 250 mM and 325 mM H 2 O 2 , and the percentage staining increased with increasing H 2 O 2 concentration. These data suggested that M. aeruginosa exposed to H 2 O 2 underwent an apoptotic event. Additionally, cells exposed to H 2 O 2 had increased cytoplasmic vacuolation and nontypical DNA laddering. Increased caspase-3-like activity was not inhibited in the presence of the synthetic caspase inhibitor carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone. Therefore, H 2 O 2 induced apoptotic-like cell death in a dose-dependent manner. Taken together, our results provided a novel mechanism for explaining cyanobacterial bloom dynamics in response to environmental stress. The results also contributed to the understanding of the origin and evolution of programmed cell death.

KMnO 4 –Fe(II) pretreatment to enhance Microcystis aeruginosa removal by aluminum coagulation: Does it work after long distance transportation?

“…The damage of algae cells was attributed to the oxidative effect of KMnO 4 rather than that of the in-situ MnO 2 . Chemical oxidants such as H 2 O 2 have been reported to induce oxidative stress to algae cells and cause the programmed cell death (PCD) of algae cells (Ross et al, 2006;Ding et al, 2012;Mikula et al, 2012), and this effect can induce the rapid collapse of M. aeruginosa bloom (Kaneko et al, 2007;Frangeul et al, 2008). PCD is a genetically controlled form of cell suicide (Ameisen, 2002), which could be induced by heat, nutrient deprivation, salt stress, ultraviolet irradiation, and oxidative stress (Bidle and Falkowski, 2004;Bidle et al, 2007).…”

Programmed cell death in the cyanobacterium Microcystis aeruginosa induced by allelopathic effect of submerged macrophyte Myriophyllum spicatum in co-culture system

“…However, little molecular biological information is available on PCD in M. aeruginosa. Experimental evidence for caspase-3-like proteases in cyanobacteria has been obtained primarily from the studies on the effect of adverse environmental factors thought to induce PCD such as treatment of the cyanobacterium M. aeruginosa with H 2 O 2 (Ding et al 2012), exposure of the freshwater cyanobacterium Anabaena sp. to univalent cation salts (Ning et al 2002), and subjection of Trichodesmium sp.…”

“…Similar results have been reported for the cyanobacteria Anabaena sp. PCC7120 (Ning et al 2002) and M. aeruginosa (Ding et al 2012). Disintegration of ultrastructure is another hallmark of PCD and includes vacuolization and degradation of internal cellular components, although plasma membranes remain intact in prokaryotic cells (Berman-Frank et al 2004).…”

“…Sustained exposure to TPC leads to formation of excess ROS/NO that triggers PCD in M. aeruginosa. Ross et al (2006) reported that caspase-3-like activity was elicited in M. aeruginosa in the wild environment treated with H 2 O 2 , and Ding et al (2012) contributed to our understanding of PCD in M. aeruginosa by describing the diverse PCD markers that appeared after exposure to H 2 O 2 . It is well known that ROS can directly react with biomolecules and damage DNA, proteins (enzymes), lipids (membranes), etc.…”

“…The DNA was then stained with GelRed (Biotium, catalog no. 41003, 0.5 mL) and analyzed by gel electrophoresis with 0.8 % agarose prepared in 0.5× TBE buffer (10× TBE was 0.89 M Tris, 0.89 M boric acid, and 20 mM Na 2 EDTA, pH 8.3) at 100 V for 30 min (Ding et al 2012). …”