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首页> 外文期刊>Anticancer Research: International Journal of Cancer Research and Treatment >Hydroquinone-induced apoptosis in HL-60 cells.
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Hydroquinone-induced apoptosis in HL-60 cells.

机译：对苯二酚诱导的HL-60细胞凋亡。

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摘要

To clarify the mechanisms by which hydroquinone (HQ; 1,4-benzenediol) produces apoptosis, HQ-induced cytotoxicity, intemucleosomal DNA fragmentation, activation of superoxide dismutase (SOD), expression of Mn and Cu/ZnSOD mRNA and activation of caspase-3, -8 and -9 were investigated in the human promyelocytic leukemic cell line HL-60. Electrophoresis and activity staining of the SOD-enriched fraction showed that HQ reduced MnSOD activation more than Cu/ZnSOD activation, suggesting that it induces mitochondrial dysfunction at an early stage of apoptosis. Furthermore, the expression of MnSOD mRNA was suppressed to a greater extent than that of Cu/ZnSOD mRNA, implying that HQ causes apoptosis by inhibiting MnSOD induction. Release of cytochrome c and activation of procaspase-3 and -9, but not of procaspase-8, occurred more rapidly (as early as 6 h) in HQ-treated cells, suggesting that HQ activates the intrinsic pathway of apoptosis. Addition of the antioxidant N-acetyl-L-cysteine (NAC) significantly reduced the cytotoxicity of HQ. At a concentration that was cytotoxic to 50% of the cells (approximately 0.05 mM), HQ activated caspase-3; this effect was reduced in the presence of NAC. Interestingly, higher concentrations of HQ (0.1-0.2 mM) caused direct cell death; however, when combined with 5 mM NAC, the activation of caspase-3 was strongly enhanced, suggesting the promotion of apoptosis. The activation of caspase-3 by HQ/NAC combinations suggests that NAC, a precursor of intracellular glutathione synthesis, acts as a co-catalyst during HQ-induced apoptosis.
机译：为了阐明氢醌（HQ; 1，4-苯二醇）产生凋亡的机制，HQ诱导的细胞毒性，核糖体间DNA片段化，超氧化物歧化酶（SOD）的活化，Mn和Cu ​​/ ZnSOD mRNA的表达以及caspase-3的活化在人早幼粒细胞白血病细胞系HL-60中研究了-8，-9。富集SOD的级分的电泳和活性染色表明，HQ降低的MnSOD激活比Cu / ZnSOD的激活更多，这表明它在凋亡的早期诱导线粒体功能障碍。此外，与Cu / ZnSOD mRNA的表达相比，MnSOD mRNA的表达被更大程度地抑制，这暗示HQ通过抑制MnSOD诱导而引起细胞凋亡。在HQ处理的细胞中，细胞色素c的释放和procaspase-3和-9的激活（而不是procaspase-8的激活）在HQ处理的细胞中发生得更快（最早6小时），这表明HQ激活了细胞凋亡的内在途径。添加抗氧化剂N-乙酰基-L-半胱氨酸（NAC）可以显着降低HQ的细胞毒性。在对50％的细胞具有细胞毒性的浓度下（约0.05 mM），HQ激活了caspase-3。在NAC的存在下，这种作用减弱了。有趣的是，较高的HQ浓度（0.1-0.2 mM）导致细胞直接死亡。但是，当与5 mM NAC结合使用时，caspase-3的激活会大大增强，提示细胞凋亡的促进。 HQ / NAC组合对caspase-3的激活表明，NAC是细胞内谷胱甘肽合成的前体，在HQ诱导的细胞凋亡过程中充当助催化剂。

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