Effects of Menadione, Hydrogen Peroxide, and Quercetin on Apoptosis and Delayed Luminescence of Human Leukemia Jurkat T-Cells
Effects of Menadione, Hydrogen Peroxide, and Quercetin on Apoptosis and Delayed Luminescence of Human Leukemia Jurkat T-Cells
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DOI：
10.1007/s12013-010-9104-1
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发表时间：
2010-12-01
影响因子：
2.6
通讯作者：
Ursaciuc, Cornel
中科院分区：
文献类型：
--
作者：
Baran, Irina;Ganea, Constanta;Ursaciuc, Cornel
甲苯二酮(MD)是一种有效的细胞毒性药物，能在细胞内产生大量的超氧阴离子。栎素(QC)是一种分布广泛的生物黄酮类化合物，具有抗氧化和促氧化双重作用，对不同类型的癌细胞具有特异性抑制细胞增殖和诱导细胞凋亡的作用。我们研究了紫外光诱导的延迟发光与MD、H_2O_2、QC对人白血病Jurkat T细胞凋亡和细胞周期的影响。500 mU M H(2)O(2)和250 mU M MD处理20分钟后，细胞凋亡率分别为66.0+/-A4.9和46.4+/-A8.6%。长期(24 H)预先接触5 mU M可促进MD诱导的细胞凋亡，而短期(1 H)预先加入10 mU M QC对H(2O)O(2)诱导的细胞凋亡有50%的保护作用，但可增强MD诱导的细胞凋亡。由于血液中QC的生理水平通常低于10微米，这些数据可以提供有关黄酮类药物联合治疗白血病的益处的相关信息。三种药物对糖尿病视网膜病变均有显著影响。我们的数据与(1)线粒体呼吸链复合体I参与了10亩S-10ms尺度上延迟发光的重要来源，(2)超氧阴离子在100亩S-10ms尺度上猝灭DL的能力，可能是通过抑制复合体I中Fe/S中心的反向电子转移，以及(3)DL对细胞内OH和H(2)O(2)水平的相对不敏感。
Menadione (MD) is an effective cytotoxic drug able to produce intracellularly large amounts of superoxide anion. Quercetin (QC), a widely distributed bioflavonoid, can exert both antioxidant and pro-oxidant effects and is known to specifically inhibit cell proliferation and induce apoptosis in different cancer cell types. We have investigated the relation between delayed luminescence (DL) induced by UV-laser excitation and the effects of MD, hydrogen peroxide, and QC on apoptosis and cell cycle in human leukemia Jurkat T-cells. Treatments with 500 mu M H(2)O(2) and 250 mu M MD for 20 min produced 66.0 +/- A 4.9 and 46.4 +/- A 8.6% apoptotic cell fractions, respectively. Long-term (24 h) pre-exposure to 5 mu M, but not 0.5 mu M QC enhanced apoptosis induced by MD, whereas short-term (1 h) pre-incubation with 10 mu M QC offered 50% protection against H(2)O(2)-induced apoptosis, but potentiated apoptosis induced by MD. Since physiological levels of QC in the blood are normally less than 10 mu M, these data can provide relevant information regarding the benefits of flavonoid-combined treatments of leukemia. All the three drugs exerted significant effects on DL. Our data are consistent with (1) the involvement of Complex I of the mitochondrial respiratory chain as an important source of delayed light emission on the 10 mu s-10 ms scale, (2) the ability of superoxide anions to quench DL on the 100 mu s-10 ms scale, probably via inhibition of reverse electron transfer at the Fe/S centers in Complex I, and (3) the relative insensitivity of DL to intracellular OH(aEuro cent) and H(2)O(2) levels.