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首页> 外文期刊>Journal of biological inorganic chemistry: JBIC: a publication of the Society of Biological Inorganic Chemistry >Selenite-mediated production of superoxide radical anions in A549 cancer cells is accompanied by a selective increase in SOD1 concentration, enhanced apoptosis and Se-Cu bonding
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Selenite-mediated production of superoxide radical anions in A549 cancer cells is accompanied by a selective increase in SOD1 concentration, enhanced apoptosis and Se-Cu bonding

机译：亚硒酸盐介导的A549癌细胞中超氧自由基阴离子的产生伴随SOD1浓度的选择性增加，细胞凋亡和Se-Cu键的选择性增加

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摘要

Selenite may exert its cytotoxic effects against cancer cells via the generation of reactive oxygen species (ROS). We investigated sources of, and the cellular response to, superoxide radical anion (O_2~(.-)) generated in human A549 lung cancer cells after treatment with selenite. A temporal delay was observed between selenite treatment and increases in O_2~(.-) production and biomarkers of apoptosisecrosis, indicating that the reduction of selenite by the glutathione reductase/NADPH system (yielding O_2~(.-)) is a minor contributor to ROS production under these conditions. By contrast, mitochondrial and NADPH oxidase O_2~(.-) generation were the major contributors. Treatment with a ROS scavenger [poly(ethylene glycol)- conjugated superoxide dismutase (SOD) or sodium 4,5- dihydroxybenzene-1,3-disulfonate] 20 h after the initial selenite treatment inhibited both ROS generation and apoptosis determined at 24 h. In addition, SOD1 was selectively upregulated and its perinuclear cytoplasmic distribution was colocalised with the cellular distribution of selenium. Interestingly, messenger RNA for manganese superoxide dismutase, catalase, inducible haem oxygenase 1 and glutathione peroxidase either remained unchanged or showed a delayed response to selenite treatment. Colocalisation of Cu and Se in these cells (Weekley et al. in J. Am. Chem. Soc. 133:18272-18279, 2011) potentially results from the formation of a Cu-Se species, as indicated by Cu K-edge extended X-ray absorption fine structure spectra. Overall, SOD1 is upregulated in response to selenite- mediated ROS generation, and this likely leads to an accumulation of toxic hydrogen peroxide that is temporally related to decreased cancer cell viability. Increased expression of SOD1 gene/protein coupled with formation of a Cu-Se species may explain the colocalisation of Cu and Se observed in these cells.
机译：亚硒酸盐可能通过产生活性氧（ROS）来发挥其对癌细胞的细胞毒性作用。我们研究了亚硒酸盐治疗后人A549肺癌细胞中产生的超氧自由基阴离子（O_2〜（.-））的来源及其对细胞的反应。在亚硒酸盐处理和O_2〜（.-）产量增加​​以及凋亡/坏死的生物标志物之间观察到时间延迟，这表明谷胱甘肽还原酶/ NADPH系统（产生O_2〜（.-））减少亚硒酸盐是次要的。在这些条件下有助于产生ROS。相比之下，线粒体和NADPH氧化酶O_2〜（.-）的生成是主要的贡献者。初始亚硒酸盐处理后20小时，用ROS清除剂[聚（乙二醇）-共轭超氧化物歧化酶（SOD）或4,5-二羟基苯-1,3-二磺酸钠]处理可抑制ROS的产生和24小时测定的细胞凋亡。此外，SOD1被选择性上调，其核周细胞质分布与硒的细胞分布共定位。有趣的是，锰过氧化物歧化酶，过氧化氢酶，诱导型血红素加氧酶1和谷胱甘肽过氧化物酶的信使RNA保持不变或对亚硒酸盐处理的反应延迟。这些细胞中Cu和Se的共定位（Weekley等人，J。Am。Chem。Soc。133：18272-18279，2011）可能是由于形成了Cu-Se物种所致， X射线吸收精细结构光谱。总体而言，SOD1响应亚硒酸盐介导的ROS生成而上调，这可能导致有毒的过氧化氢的积累，这在时间上与癌细胞活力的降低有关。 SOD1基因/蛋白质表达的增加与Cu-Se物种的形成可能解释了在这些细胞中观察到的Cu和Se的共定位。

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