Hydrogen peroxide induces apoptotic-like cell death in Microcystis aeruginosa (Chroococcales, Cyanobacteria) in a dose-dependent manner
Hydrogen peroxide induces apoptotic-like cell death in Microcystis aeruginosa (Chroococcales, Cyanobacteria) in a dose-dependent manner
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DOI：
10.2216/11-107.1
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发表时间：
2012-09-01
期刊：
影响因子：
1.6
通讯作者：
Song, Lirong
中科院分区：
文献类型：
--
作者：
Ding, Yi;Gan, Nanqin;Song, Lirong
我们通过对铜绿微囊藻暴露于过氧化氢后的形态、分子和生理特性的研究，探讨了铜绿微囊藻诱导细胞凋亡的能力。150 mU H_2O_2对微囊藻的增殖影响较小，250和325 mU H_2O_2对微囊藻细胞数量有明显的抑制作用。用透射电子显微镜观察250和325mU H_2O_2对细胞的作用，发现细胞膜变形，类囊体部分解体。相应地，Hoechst 33342染色的荧光成像显示了类核染色质的凝聚。此外，在250和325 mU M H_2O_2暴露后，细胞损伤伴随着光合作用效率(可变荧光与最大荧光的比值[Fv/Fm]、最大电子传递速率[ETRmax])的显著降低和类caspase-3活性的升高。在250 mU和325 mU H_2O_2作用下，细胞出现末端脱氧核苷酸转移酶5-三磷酸缺口末端标记阳性染色，且染色百分率随H_2O_2浓度的增加而增加。这些数据表明，暴露在过氧化氢中的铜绿假单胞菌经历了一次细胞凋亡事件。此外，暴露于H_2O_2的细胞出现细胞质空泡化和非典型DNA梯状条带。合成的半胱氨酸天冬氨酸酶抑制剂carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone.不能抑制半胱氨酸酶-3样活性的增加因此，过氧化氢以剂量依赖的方式诱导类凋亡性细胞死亡。综上所述，我们的结果为解释蓝藻水华对环境胁迫的响应提供了一种新的机制。这些结果也有助于理解细胞程序性死亡的起源和进化。
We investigated the capability of Microcystis aeruginosa to cause apoptosis by pursuing morphological, molecular and physiological characteristics after exposure to H2O2. Microcystis proliferation was only weakly affected after exposure to 150 mu M H2O2 but cell numbers decreased dramatically after exposures of 250 and 325 mu M H2O2. Cells exposed to 250 and 325 mu M H2O2 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 mu M H2O2. Terminal deoxynucleotidyl transferase Deoxyuridine 5-triphosphate nick end labelling (TUNEL) positive staining appeared in cells exposed to 250 mu M and 325 mu M H2O2, and the percentage staining increased with increasing H2O2 concentration. These data suggested that M. aeruginosa exposed to H2O2 underwent an apoptotic event. Additionally, cells exposed to H2O2 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, H2O2 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.