H2O2-induced block of glycolysis as an active ADP-ribosylation reaction protecting cells from apoptosis
H2O2-induced block of glycolysis as an active ADP-ribosylation reaction protecting cells from apoptosis
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DOI：
10.1096/fj.00-0074com
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发表时间：
2000-11-01
期刊：
影响因子：
4.8
通讯作者：
Ghibelli, L
中科院分区：
文献类型：
--
作者：
Colussi, C;Albertini, MC;Ghibelli, L
H2 O2处理U937细胞导致糖酵解通量的阻断和甘油醛-3-磷酸脱氢酶的翻译后修饰失活（可能是ADP-核糖基化），糖酵解在从氧化应激恢复2小时后自发地重新激活;此后细胞开始经历凋亡，特异性ADP核糖基化抑制剂3-氨基苯甲酰胺抑制应激诱导的甘油醛-3-磷酸脱氢酶失活和糖酵解阻断;同时，它预期并增加细胞凋亡，糖酵解的外源性阻断（即，通过在无葡萄糖培养基中培养或与葡萄糖类似物一起培养或在NAD耗尽后培养），将瞬时阻断转变为稳定阻断：这导致保护免于细胞凋亡，即使当下游细胞代谢通过加入丙酮酸盐保持活性时也是如此。所有这些证据表明应激诱导的糖酵解阻断不是被动氧化损伤的结果，而是通过ADP核糖基化进行细胞自我防御的活跃细胞反应。科卢西角，Albertini，M. C.的方法，科波拉，S.，Rovidati，S.，Galli，F.，吉贝利湖H2 O2诱导的糖酵解阻断是一种保护细胞免于凋亡的主动ADP-核糖基化反应。
H2O2 treatment on U937 cells leads to the block of glycolytic flux and the inactivation of glyceraldehyde-3-phosphate-dehydrogenase by a posttranslational modification (possibly ADP-ribosylation), Glycolysis spontaneously reactivates after 2 h of recovery from oxidative stress; thereafter cells begin to undergo apoptosis, The specific ADP-ribosylation inhibitor 3-aminobenzamide inhibits the stress-induced inactivation of glyceraldehyde-3-phosphate-dehydrogenase and the block of glycolysis; concomitantly, it anticipates and increases apoptosis, Exogenous block of glycolysis (i.e., by culture in glucose-free medium or with glucose analogs or after NAD depletion), turns the transient block into a stable one: this results in protection from apoptosis, even when downstream cell metabolism is kept active by the addition of pyruvate, All this evidence indicates that the stress-induced block of glycolysis is not the result of a passive oxidative damage, but rather an active cell reaction programmed via ADP-ribosylation for cell self-defense.-Colussi, C., Albertini, M. C., Coppola, S., Rovidati, S., Galli, F., Ghibelli, L. H2O2-induced block of glycolysis as an active ADP-ribosylation reaction protecting cells from apoptosis.