Inhibition of poly(ADP-ribose) polymerase preserves surfactant synthesis after hydrogen peroxide exposure.
Inhibition of poly(ADP-ribose) polymerase preserves surfactant synthesis after hydrogen peroxide exposure.
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聚（ADP-核糖）聚合酶的抑制可在过氧化氢暴露后保留表面活性剂的合成。
DOI：
10.1152/ajplung.1995.269.1.l59
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Holm,BA
中科院分区：
文献类型：
--
作者：
Hudak,BB;Tufariello,J;Sokolowski,J;Maloney,C;Holm,BA
暴露于过氧化氢 (H2O2) 会降低兔 II 型肺细胞中磷脂酰胆碱 (PC) 的合成。聚（ADP-核糖）聚合酶（PARP）的激活可能在此过程中发挥作用。 II 型肺细胞暴露于 H2O2 导致 [3H]胆碱掺入 PC 的速率降低 53%（P < 0.001）。细胞 NAD 和 ATP 水平分别降低 52% (P < 0.001) 和 39% (P < 0.01)，但细胞活力没有显着变化。暴露于 H2O2 还导致 PARP 活性增加 52% (P < 0.05)。在暴露于 H2O2 之前将 II 型细胞与 PARP 抑制剂（烟酰胺；3-氨基苯甲酰胺）预孵育可防止 PARP 活性的增加，并阻止 ATP、NAD 和 PC 合成速率的下降。这些结果表明，与 PARP 激活相关的能量消耗导致氧化应激对 II 型细胞代谢功能的影响，并且可以通过体外药物来改善。
Exposure to hydrogen peroxide (H2O2) decreases phosphatidylcholine (PC) synthesis in rabbit type II pneumocytes. Activation of poly(ADP-ribose) polymerase (PARP) may play a role in this process. Exposure of type II pneumocytes to H2O2 resulted in a 53% decrease in the rate of incorporation of [3H]choline into PC (P < 0.001). Cell NAD and ATP levels were decreased by 52% (P < 0.001) and 39% (P < 0.01), respectively, without significant changes in cell viability. Exposure to H2O2 also resulted in a 52% (P < 0.05) increase in the activity of PARP. Preincubation of type II cells with inhibitors of PARP (nicotinamide; 3-aminobenzamide) before H2O2 exposure prevented the increase in PARP activity, and blocked the decreases in ATP, NAD, and rate of PC synthesis. These results suggest that the energy depletion associated with activation of PARP contributes to the effects of oxidant stress on type II cell metabolic function and may be ameliorated by pharmacological agents in vitro.