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首页> 外文期刊>Journal of biochemical and molecular toxicology >Differential effect of ascorbic acid and n-acetyl-L-cysteine on arsenic trioxide-mediated oxidative stress in human leukemia (HL-60) cells.
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Differential effect of ascorbic acid and n-acetyl-L-cysteine on arsenic trioxide-mediated oxidative stress in human leukemia (HL-60) cells.

机译：抗坏血酸和正乙酰基-L-半胱氨酸对三氧化二砷介导的人类白血病（HL-60）细胞氧化应激的差异作用。

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Arsenic trioxide (ATO) has been recommended for the treatment of refractory cases of acute promyelocytic leukemia (APL). Recent studies in our laboratory indicated that oxidative stress plays a key role in ATO-induced cytotoxicity in human leukemia (HL-60) cells. In the present investigation, we performed the MTT assay and trypan blue exclusion test for cell viability. We also performed the thiobarbituric acid test to determine the levels of malondialdehyde (MDA) production in HL-60 cells coexposed to either ascorbic acid (AA) and ATO or to n-acetyl-L-cysteine (NAC) and ATO. The results of MTT assay indicated that AA exposure potentiates the cytotoxicity of ATO in HL-60 cells, as evidenced by a gradual increase in MDA levels with increasing doses of AA. In contrary, the addition of NAC to ATO-treated HL-60 cells resulted in a dose-dependent decrease of MDA production. From these results, we conclude that the addition of the AA to ATO-treated HL-60 cells enhances the formation of reactive oxygen species(ROS), whereas the addition of NAC under the same experimental condition significantly (p .05) decreases the level of ROS formation. On the basis of these direct in vitro findings, our studies provide evidence that AA may extend the therapeutic spectrum of ATO. The coadministration of NAC with ATO shows a potential specificity for tumor cells, indicating that it may not enhance the clinical outcome associated with ATO monotherapy in vivo.
机译：三氧化二砷（ATO）已被推荐用于治疗难治性急性早幼粒细胞白血病（APL）。我们实验室的最新研究表明，氧化应激在ATO诱导的人白血病（HL-60）细胞毒性中起着关键作用。在本研究中，我们进行了MTT分析和锥虫蓝排除测试，以检测细胞的生存能力。我们还进行了硫代巴比妥酸测试，以确定与抗坏血酸（AA）和ATO或正乙酰基-L-半胱氨酸（NAC）和ATO共同暴露的HL-60细胞中丙二醛（MDA）产生的水平。 MTT测定的结果表明，AA暴露增强了HL-60细胞中ATO的细胞毒性，这是通过随着AA剂量的增加MDA水平的逐渐升高来证明的。相反，向ATO处理的HL-60细胞中添加NAC导致MDA产生的剂量依赖性降低。根据这些结果，我们得出结论，在ATO处理的HL-60细胞中添加AA可以增强活性氧（ROS）的形成，而在相同的实验条件下添加NAC则可以显着降低（p <.05）。 ROS形成水平。基于这些直接的体外研究结果，我们的研究提供了证据，即AA可以扩展ATO的治疗范围。 NAC与ATO的共同给药显示了对肿瘤细胞的潜在特异性，表明它可能不会增强与ATO体内单一疗法相关的临床结果。

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