...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >The effect of bicarbonate on menadione-induced redox cycling and cytotoxicity: Potential involvement of the carbonate radical
【24h】

The effect of bicarbonate on menadione-induced redox cycling and cytotoxicity: Potential involvement of the carbonate radical

机译：碳酸氢盐对甲萘醌诱导的氧化还原循环和细胞毒性的影响：碳酸根自由基的潜在参与

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

We have investigated the effect of NaHCO3 on menadione redox cycling and cytotoxicity. A cell-free system utilized menadione and ascorbic acid to catalyze a redox cycle, and we utilized murine hepatoma (Hepa 1c1c7) cells for in vitro experiments. Experiments were performed using low (2 mmol/L) and physiological (25 mmol/L) levels of NaHCO3 in buffer equilibrated to physiological pH. Using oximetry, ascorbic acid oxidation, and ascorbyl radical detection, we found that menadione redox cycling was enhanced by NaHCO3. Furthermore, Hepa 1c1c7 cells treated with menadione demonstrated cytotoxicity that was significantly increased with physiological concentrations of NaHCO3 in the media, compared with low levels of NaHCO3. Interestingly, the inhibition of superoxide dismutase (SOD) with 2 different metal chelators was associated with a protective effect against menadione cytotoxicity. Using isolated protein, we found a significant increase in protein carbonyls with menadione-ascorbate-SOD with physiological NaHCO3 levels; low NaHCO3 or SOD-free reactions produced lower levels of protein carbonyls. In conclusion, these findings suggest that the hydrogen peroxide generated by menadione redox cycling together with NaHCO3-CO2 are potential substrates for SOD peroxidase activity that can lead to carbonate-radical-enhanced cytotoxicity. These findings demonstrate the importance of NaHCO3 in menadione redox cycling and cytotoxicity.
机译：我们已经研究了NaHCO3对甲萘醌氧化还原循环和细胞毒性的影响。一个无细胞的系统利用甲萘醌和抗坏血酸来催化氧化还原循环，我们利用鼠肝癌（Hepa 1c1c7）细胞进行体外实验。在平衡至生理pH的缓冲液中使用低（2 mmol / L）和生理（25 mmol / L）的NaHCO3水平进行实验。使用血氧测定法，抗坏血酸氧化和抗坏血酸自由基检测，我们发现NaHCO3增强了甲萘醌氧化还原循环。此外，与低水平的NaHCO3相比，用甲萘醌处理的Hepa 1c1c7细胞表现出的细胞毒性随着培养基中NaHCO3的生理浓度而显着增加。有趣的是，用2种不同的金属螯合剂抑制超氧化物歧化酶（SOD）与针对甲萘醌细胞毒性的保护作用有关。使用分离的蛋白质，我们发现具有生理性NaHCO3水平的甲萘醌-抗坏血酸-SOD显着增加了蛋白质羰基的含量;低的NaHCO3或无SOD的反应产生的蛋白质羰基含量较低。总之，这些发现表明，甲萘醌氧化还原循环与NaHCO3-CO2一起产生的过氧化氢是SOD过氧化物酶活性的潜在底物，可导致碳酸盐自由基增强的细胞毒性。这些发现证明了NaHCO 3在甲萘醌氧化还原循环和细胞毒性中的重要性。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号