Dzyubinskaya E V, Kiselevsky D B, Lobysheva N V, Shestak A A, Samuilov V D
Faculty of Biology, Lomonosov Moscow State University, Moscow, 119992, Russia.
Biochemistry (Mosc). 2006 Oct;71(10):1120-7. doi: 10.1134/s0006297906100105.
Cyanide is an apoptosis inducer in stoma guard cells from pea leaf epidermis. Unlike CN-, the uncoupler of oxidative and photosynthetic phosphorylation carbonyl cyanide m-chlorophenylhydrazone (CCCP), the combination of CCCP, 3-(3 ,4 -dichlorophenyl)-1,1-dimethylurea (DCMU), benzylhydroxamate (BH), myxothiazol, antimycin A, and a glycolysis inhibitor 2-deoxyglucose (DG) did not induce destruction of guard cell nuclei for 20 h of incubation of epidermal peels in the light. DCMU prevented the effect of CN- as a programmed cell death (PCD) inducer. CCCP, the combination of DCMU and CCCP, or the combination of DCMU, CCCP, BH, myxothiazol, antimycin A, and DG supplemented by CN- caused destruction of cell nuclei; the number of the cells lacking nuclei in this case was higher than with CN- alone. DG and CCCP caused cell destruction after longer incubation of the isolated epidermis - after 2 days and to a greater degree after 4 days. The effect of DG and CCCP was reduced by illumination. Cell destruction during long-term incubation was prevented by the combination of DG and CCCP. From data of electron microscopy, DCMU and dinitrophenyl ester of iodonitrothymol (DNP-INT) prevented apoptotic changes of the nuclear ultrastructure induced by CN-. The suppression of the destruction of the guard cell nuclei under combined action of DG and CCCP was apparently caused by switching of cell death from PCD to necrosis. Thus, the type of cell death - via apoptosis or necrosis - is controlled by the level of energy provision.
氰化物是豌豆叶表皮气孔保卫细胞中的一种凋亡诱导剂。与氧化磷酸化和光合磷酸化解偶联剂羰基氰化物间氯苯腙（CCCP）不同，CCCP、3-(3,4-二氯苯基)-1,1-二甲基脲（DCMU）、苄基羟肟酸（BH）、粘噻唑、抗霉素A和糖酵解抑制剂2-脱氧葡萄糖（DG）的组合在光照下孵育表皮条20小时并未诱导保卫细胞核的破坏。DCMU可阻止CN-作为程序性细胞死亡（PCD）诱导剂的作用。CCCP、DCMU与CCCP的组合，或DCMU、CCCP、BH、粘噻唑、抗霉素A和DG并补充CN-的组合会导致细胞核破坏；在这种情况下，缺乏细胞核的细胞数量比单独使用CN-时更高。DG和CCCP在分离的表皮孵育较长时间后——2天后——会导致细胞破坏，4天后破坏程度更大。光照可降低DG和CCCP的作用。DG和CCCP的组合可防止长期孵育期间的细胞破坏。从电子显微镜数据来看，DCMU和碘硝基百里酚二硝基苯酯（DNP-INT）可阻止CN-诱导的核超微结构的凋亡变化。DG和CCCP联合作用下保卫细胞核破坏的抑制显然是由于细胞死亡从PCD转变为坏死所致。因此，细胞死亡的类型——通过凋亡还是坏死——由能量供应水平控制。
