• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The Journal of Nutritional Biochemistry >Copper deficiency inhibits Ca(2+)-induced swelling in rat cardiac mitochondria
【24h】

Copper deficiency inhibits Ca(2+)-induced swelling in rat cardiac mitochondria

机译：铜缺乏抑制大鼠心脏线粒体中Ca（2+）引起的肿胀

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

Cu deficiency disrupts the architecture of mitochondria, impairs respiration, and inhibits the activity of cytochrome c oxidase - the terminal, Cu-dependent respiratory complex (Complex IV) of the electron transport chain. This suggests that perturbations in the respiratory chain may contribute to the changes in mitochondrial structure caused by Cu deficiency. This study investigates the effect of Cu deficiency on Ca(2+)-induced mitochondrial swelling as it relates to changes in respiratory complex activities in cardiac mitochondria of rats. Male weanling rats were fed diets containing either no added Cu (Cu0), 1.5 mg Cu/kg (Cu1.5), 3 mg Cu/kg (Cu3) or 6 mg Cu/kg (Cu6). The rate of Ca(2+)-induced mitochondrial swelling in the presence of succinate and oligomycin was reduced, and the time to reach maximal swelling was increased only in the rats consuming Cu0 diet. Cytochrome c oxidase activity was reduced 60% and 30% in rats fed Cu0 and Cu1.5, respectively, while NADH:cytochrome c reductase (Complex I+ComplexIII) activity was reduced 30% in rats consuming both Cu0 and Cu1.5. Mitochondrial swelling is representative of mitochondrial permeability transition pore (MPTP) formation and the results suggest that Ca(2+)-induced MPTP formation occurs in cardiac mitochondria of Cu-deficient rats only when cytochrome c oxidase activity falls below 30% of normal. Decreased respiratory complex activities caused by severe Cu deficiency may inhibit MPTP formation by increasing matrix ADP concentration or promoting oxidative modifications that reduce the sensitivity of the calcium trigger for MPTP formation.
机译：铜缺乏会破坏线粒体的结构，损害呼吸，并抑制细胞色素c氧化酶（电子传输链末端依赖铜的呼吸道复合物（复合物IV））的活性。这表明呼吸链中的扰动可能是由于铜缺乏引起的线粒体结构变化的原因。这项研究调查了铜缺乏对Ca（2+）诱导的线粒体肿胀的影响，因为它与大鼠心脏线粒体中呼吸复合物活性的变化有关。给雄性断奶大鼠饲喂不添加Cu（Cu0），1.5 mg Cu / kg（Cu1.5），3 mg Cu / kg（Cu3）或6 mg Cu / kg（Cu6）的饮食。 Ca（2+）诱导的琥珀酸和寡霉素存在下线粒体肿胀的速率降低，并且达到最大肿胀的时间仅在食用Cu0饮食的大鼠中增加。进食Cu0和Cu1.5的大鼠的细胞色素c氧化酶活性分别降低60％和30％，而同时摄入Cu0和Cu1.5的大鼠的NADH：细胞色素c还原酶（Complex I + ComplexIII）活性降低30％。线粒体肿胀代表线粒体通透性过渡孔（MPTP）的形成，结果表明Ca（2+）诱导的MPTP形成仅在细胞色素C氧化酶活性低于正常值的30％时在缺铜大鼠的心脏线粒体中发生。严重的铜缺乏引起的呼吸系统复杂活动减少可能会通过增加基质ADP浓度或促进氧化修饰而抑制MPTP形成，从而降低钙触发物对MPTP形成的敏感性。

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