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目的探讨缺氧和氰化物中毒2种因素对大鼠脑线粒体能量储备和线粒体复合体抑制的作用。方法雄性SD大鼠分为平原组、高原急性缺氧组和阶梯适应组。各组大鼠进行相应的处理后,腹腔注射氰化钠3.6mg/kg,于中毒0,0.5和2h时相点麻醉,断头取脑,提取脑组织线粒体蛋白。高效液相色谱分析大鼠脑线粒体腺苷三磷酸(ATP)、腺苷二磷酸(ADP)和腺苷一磷酸(AMP)含量。常规比色法测定线粒体呼吸链复合体Ⅰ和Ⅳ的活性。结果平原组、高原缺氧组和阶梯适应组氰化钠中毒脑内线粒体ATP的含量降低,ADP和AMP的含量增加(P<0.05或P<0.01);线粒体复合体Ⅰ和Ⅳ的活性降低,与对照组比较差异有统计学意义(P<0.01);高原缺氧组与相应的平原组比较脑内线粒体ATP的含量降低(P<0.05),ADP和AMP的含量增加(P<0.05)。结论氰化钠中毒可加重急性高原缺氧导致的脑组织线粒体内腺苷酸能量代谢储备障碍和线粒体复合体Ⅰ和Ⅳ活性抑制。
Objective To investigate the effects of hypoxia and cyanide poisoning on the mitochondrial energy storage and mitochondrial complex inhibition in rats. Methods Male SD rats were divided into plain group, acute hypoxia group and step adaptation group. After corresponding treatment, rats in each group were intraperitoneally injected with 3.6 mg / kg of sodium cyanide, anesthetized at 0, 0.5, and 2 h, and their brains were removed by decapitation to extract mitochondrial protein. The contents of adenosine triphosphate (ATP), adenosine diphosphate (ADP) and adenosine monophosphate (AMP) in rat brain were analyzed by high performance liquid chromatography. Routine colorimetric assay of mitochondrial respiratory chain complex Ⅰ and Ⅳ activity. Results The content of ATP in mitochondria decreased and the content of ADP and AMP increased (P <0.05 or P <0.01), the activity of mitochondrial complex I and IV decreased in the plateau group, plateau hypoxia group and ladder adaptation group, Compared with the control group, the difference was statistically significant (P <0.01). Compared with the control group, the level of mitochondrial ATP in the anoxic plateau decreased (P <0.05) and the content of ADP and AMP increased (P <0.05). Conclusion Sodium cyanide poisoning can aggravate the disturbance of energy metabolism reserve of mitochondrial adenylate energy metabolism and mitochondrial complex Ⅰ and Ⅳ activity induced by hypoxia in the plateaus.