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首页> 外文期刊>Cell biology international. >Fructose sensitizes Jurkat cells oxidative stress-induced apoptosis via caspase-dependent and caspase-independent mechanisms
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Fructose sensitizes Jurkat cells oxidative stress-induced apoptosis via caspase-dependent and caspase-independent mechanisms

机译：果糖通过caspase依赖性和caspase依赖性机制敏化Jurkat细胞氧化应激诱导的凋亡

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Whether fructose (FRU), as the sole energy source, confers a metabolic advantage on cancer cells against noxious stimuli is unknown. The aim of this study was to evaluate the effects of low (11 mM), moderate (25 mM), and high (55mM) FRU concentrations alone or in combination with rotenone (ROT) or doxorubicin (DOX) in Jurkat cells, an acute lymphoblastic leukemia cell model. Glucose (GLU) was used as a control. Using different cell analysis techniques, we demonstrated that FRU was predominantly metabolized via oxidative phosphorylation (similar to 95%) (i.e., lactate production was reduced >120-fold), resulting in endogenous oxidative stress-induced conditions. The cells were characterized by generation of O2(center dot-) (43%)/H2O2 (40%) and activation of NF-kappa B (similar to 95-fold increase, fi), c-Jun-N terminal kinase (JNK), p53 (40-fi), and c-Jun (9-fi). In addition, we observed a loss of Delta Psi(m) (10%), activation of caspase-3 (50-fi) and apoptosis-inducing factor (AIF, 2-fi), and condensation and fragmentation of the nuclei [20% by acridine orange/ethidium bromide/Hoechst (AO/EB/H) staining, 15% by flow cytometry] compared to those of GLU 11 at 24 h. Although DOX killed Jurkat cells independent of sugar content in the culture medium, leukemic cells in low, but not high, FRU were extremely sensitive to ROT. Taken together, our findings suggest that Jurkat cells are more susceptible to cell death if forced to shift from GLU metabolism (i.e., aerobic glycolysis) to FRU metabolism (i.e., oxidative phosphorylation) after treatment with mitochondria-targeting molecules. These observations may help elucidate the cell death mechanism of leukemic cells cultured in FRU.
机译：果糖（FRU）作为唯一的能源是否赋予癌细胞抵御有害刺激的代谢优势，这一点尚不清楚。这项研究的目的是评估低（11 mM），中（25 mM）和高（55mM）FRU浓度单独或与鱼藤酮（ROT）或阿霉素（DOX）联合使用对Jurkat细胞（急性）的影响淋巴细胞白血病细胞模型。葡萄糖（GLU）用作对照。使用不同的细胞分析技术，我们证明FRU主要通过氧化磷酸化代谢（约95％）（即乳酸生成减少> 120倍），从而导致内源性氧化应激诱导的疾病。这些细胞的特征是产生O2（中心点-）（43％）/ H2O2（40％）和激活NF-κB（类似增加95倍，fi），c-Jun-N末端激酶（JNK ），p53（40-fi）和c-Jun（9-fi）。此外，我们观察到了Delta Psi（m）（10％）的损失，caspase-3的激活（50-fi）和凋亡诱导因子（AIF，2-fi）的损失以及细胞核的浓缩和断裂[20]。与24小时时的GLU 11相比，by啶橙/溴化乙锭/ Hoechst（AO / EB / H）染色所占的百分比为15％，流式细胞术则为15％]。尽管DOX杀死了培养基中糖含量无关的Jurkat细胞，但低但不高的FRU中的白血病细胞对ROT极为敏感。综上所述，我们的发现表明，如果用线粒体靶向分子处理后被迫从GLU代谢（即有氧糖酵解）转移到FRU代谢（即氧化磷酸化），Jurkat细胞更容易死亡。这些观察结果可能有助于阐明在FRU中培养的白血病细胞的细胞死亡机制。

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