DNA STRAND BREAKS, NAD METABOLISM, AND PROGRAMMED CELL-DEATH
DNA STRAND BREAKS, NAD METABOLISM, AND PROGRAMMED CELL-DEATH
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DOI：
10.1016/0014-4827(86)90028-5
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发表时间：
1986-06-01
影响因子：
3.7
通讯作者：
CARRERA, CJ
中科院分区：
文献类型：
--
作者：
CARSON, DA;SETO, S;CARRERA, CJ
在静止的人淋巴细胞中，DNA单链断裂、NAD代谢和细胞活力之间存在密切关系。在稳态条件下，静息淋巴细胞不断地断裂并重新连接DNA。平衡的DNA切除-修复过程伴随着用于聚（ADP-核糖）合成的NAD的成比例消耗。然而，淋巴细胞从烟酰胺再合成NAD的能力有限。淋巴细胞中DNA链断裂形成的增加，或DNA修复的阻断，加速聚（ADP-核糖）形成，并可能诱导致死性NAD和ATP耗竭。通过这种方式，淋巴细胞核中DNA单链断裂的水平与细胞质的代谢活性有关。淋巴细胞（也许还有其他细胞）的程序性清除与受损的DNA，可能代表了一种新的生理功能的聚（ADP-核糖）依赖的NAD循环。
An intimate relationship exists between DNA single-strand breaks, NAD metabolism, and cell viability in quiescent human lymphocytes. Under steady-state conditions, resting lymphocytes continually break and rejoin DNA. The balanced DNA excision-repair process is accompanied by a proportional consumption of NAD for poly(ADP-ribose) synthesis. However, lymphocytes have a limited capacity to resynthesize NAD from nicotinamide. An increase in DNA strand break formation in lymphocytes, or a block in DNA repair, accelerates poly(ADP-ribose) formation and may induce lethal NAD and ATP depletion. In this way, the level of DNA single-strand breaks in the lymphocyte nucleus is linked to the metabolic activity of the cytoplasm. The programmed removal of lymphocytes (and perhaps of other cells) with damaged DNA, may represent a novel physiologic function for poly(ADP-ribose)-dependent NAD cycling.