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目的通过观察不同浓度的NaCN对模拟高原急性低氧大鼠离体肝脏线粒体呼吸氧耗、膜电位和复合酶Ⅳ活性的影响,探讨急性低氧条件下氰化物中毒大鼠线粒体能量代谢变化特点。方法16只SD大鼠按简单完全随机分组法分为对平原照组和急性低氧组,急性低氧组大鼠暴露于低压舱内,模拟海拔5000m高原,23h/d,连续3d;对照组大鼠于常压和常氧环境中同时喂养。用差速离心法提取肝线粒体,分别在0、0.01、0.1、0.25mmol/L NaCN条件下采用Clark氧电极法测定线粒体呼吸氧耗和复合酶Ⅳ活性并计算Ⅲ态呼吸(state3respiration,ST3)、Ⅳ态呼吸(state4respiration,ST4)、呼吸控制率(respiratory control rate,RCR)、氧化磷酸化效率(oxidative phosphorylation,OPR)和复合酶Ⅳ耗氧率,用Rhodamine123法测定线粒体膜电位(the mitochondrial membrane potential,MMP)。结果0.01、0.1、0.25mmol/L NaCN均可显著抑制线粒体呼吸功能,降低线粒体膜电位,且呈剂量依赖关系。与相应NaCN浓度的对照组比较,急性低氧组线粒体功能受抑制程度显著增加。结论急性低氧加重NaCN对大鼠肝脏线粒体能量代谢的抑制作用,其机制可能与急性缺氧大鼠线粒体氧化磷酸化脱偶联、呼吸链复合体Ⅳ功能降低及线粒体膜电位改变有关。
OBJECTIVE: To investigate the effects of different concentrations of NaCN on isolated rat mitochondria respiratory oxygen consumption, membrane potential and enzyme activity in simulated hypoxia-induced acute hypoxia, and to investigate the changes of mitochondrial energy metabolism in cyanide poisoning rats under acute hypoxia. Methods Twenty-six SD rats were randomly divided into two groups according to simple randomization: acute pancreas group and acute hypoxia group. Rats in acute hypoxia group were exposed to low pressure cabin at a altitude of 5000m for 23h, Rats were fed simultaneously under normobaric and normoxic conditions. Mitochondria were extracted by differential centrifugation, and mitochondrial respiratory oxygen consumption and enzyme activity were measured by Clark’s oxygen electrode method at 0, 0.01, 0.1 and 0.25mmol / L NaCN, respectively. State3stores (ST3) (State4respiration, ST4), respiratory control rate (RCR), oxidative phosphorylation (OPR) and oxygenase activity of compound enzyme Ⅳ were measured. The mitochondrial membrane potential , MMP). Results 0.01, 0.1, 0.25mmol / L NaCN can significantly inhibit mitochondrial respiratory function, reduce mitochondrial membrane potential, and in a dose-dependent manner. Compared with the corresponding control group of NaCN concentration, mitochondrial function was significantly inhibited in acute hypoxia group. Conclusions Acute hypoxia aggravates the inhibitory effect of mitochondrial energy metabolism induced by NaCN in rats. The mechanism may be related to oxidative phosphorylation and deoxy-coupling of mitochondria, reduction of respiratory chain complex Ⅳ and mitochondrial membrane potential.