过氧化氢通过芬顿反应诱导BJAB细胞自杀
Hydrogen peroxide induces apoptosis of BJAB cells due to formation of hydroxyl radicals via intracellular iron-mediated Fenton chemistry in glucose oxidase-mediated oxidative stress
本研究的目的是确定葡萄糖氧化酶（GO）产生的过氧化氢（H2O2）是否诱导BJAB细胞的凋亡或坏死，以及哪种自由基是细胞死亡的直接介导。
我们发现GO以低浓度连续产生H2O2，类似于体内条件，并且以剂量依赖性方式降低增殖和细胞活力。
GO介导的细胞毒性由细胞凋亡引起，并且通过在H33342 /膜联蛋白V /碘化丙锭染色后监测细胞来证实。
发现线粒体膜电位降低和细胞内谷胱甘肽水平是H2O2介导的细胞凋亡中的关键事件。
另外的实验表明，H2O2通过Fenton而不是Haber-Weiss反应形成羟基自由基，从而发挥其细胞凋亡作用。此外，细胞内氧化还原活性铁而非铜参与H2O2介导的细胞凋亡。
The aim of this study was to determine if hydrogen peroxide (H2O2) generated by glucose oxidase (GO) induces apoptosis or necrosis of BJAB cells and which radical is the direct mediator of cell death.
We found that GO produced H2O2 continuously in low concentrations, similar to in vivo conditions, and decreased proliferation and cell viability in a dose-dependent manner.
The GO-mediated cytotoxicity resulted from apoptosis, and was confirmed by monitoring the cells after H33342/Annexin V/propidium iodide staining.
Decreases of mitochondrial membrane potential and intracellular glutathione level were found to be critical events in the H2O2-mediated apoptosis.
Additional experiments revealed that H2O2 exerted its apoptotic action through the formation of hydroxyl radicals via the Fenton rather than the Haber-Weiss reaction. Moreover, intracellular redox-active iron, but not copper, participated in the H2O2-mediated apoptosis.
Article in Molecules and Cells 22(1):21-9 · September 2006 with 337 Reads
Source: PubMed
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