维生素K3和维生素C单独或组合诱导白血病细胞 凋亡

 

维生素K3和维生素C单独或联合诱导的白血病细胞凋亡类似氧化应激信号机制

Vitamin K3 and vitamin C alone or in combination induced apoptosis in leukemia cells by a similar oxidative stress signalling mechanism

 

翻译:蓝山

 

背景

白血病是骨髓和血液的癌症。造成这种血液病的原因目前尚不清楚。今天,治疗白血病的一线治疗包括化疗和放射治疗。不幸的是,继发性治疗相关的急性淋巴细胞白血病可能会在化疗和/或原发性恶性肿瘤放疗后出现。

 

结果

结果表明,维生素K3 或维生素C 诱导白血病细胞凋亡的氧化应激机制涉及超氧化物阴离子自由基和过氧化氢生成, 激活NF-κB, p53, c-Jun、蛋白酶caspase-3激活和线粒体去极化导致核碎裂。JurkatK562细胞暴露于VCVK3 1000:1 10mM:10μM) 或100:1 (300μM:3μM)的比例时,细胞死亡更加突出。

 

结论

我们首次提供了体外实验证据,证明在Jurkat K562中,VK3VC以多米诺效应样机制诱导细胞凋亡,总之,这些数据表明VK3VC在治疗白血病方面应该是有用的。

 

 

 

Vitamin K3 and vitamin C alone or in combination induced apoptosis in leukemia cells by a similar oxidative stress signalling mechanism

 

Vitamin K3 and vitamin C alone or in combination induced apoptosis in leukemia cells by a similar oxidative stress signalling mechanism

Angelica R Bonilla-Porras,1 Marlene Jimenez-Del-Rio,1 and Carlos Velez-Pardocorresponding author1

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Abstract

Background

Secondary therapy-related acute lymphoblastic leukemia might emerge following chemotherapy and/or radiotherapy for primary malignancies. Therefore, other alternatives should be pursued to treat leukemia.

 

Results

 

It is shown that vitamin K3- or vitamin C- induced apoptosis in leukemia cells by oxidative stress mechanism involving superoxide anion radical and hydrogen peroxide generation, activation of NF-κB, p53, c-Jun, protease caspase-3 activation and mitochondria depolarization leading to nuclei fragmentation. Cell death was more prominent when Jurkat and K562 cells are exposed to VC and VK3 in a ratio 1000:1 (10 mM: 10 μM) or 100:1 (300 μM: 3 μM), respectively.

 

Conclusion

 

We provide for the first time in vitro evidence supporting a causative role for oxidative stress in VK3- and VC-induced apoptosis in Jurkat and K562 cells in a domino-like mechanism. Altogether these data suggest that VK3 and VC should be useful in the treatment of leukemia.

 

https://cancerci.biomedcentral.com/articles/10.1186/1475-2867-11-19