Chávez J C, Pichiule P, Boero J, Arregui A
Departamento de Ciencias Fisiológicas, Universidad Peruana Cayetano Heredia, Lima.
Neurosci Lett. 1995 Jul 7;193(3):169-72. doi: 10.1016/0304-3940(95)11692-p.
Respiratory activity and NADH CoQ reductase (complex I) and cytochrome c oxidase (complex IV) activities were measured in free (non-synaptosomal) mitochondria isolated from cerebral cortex of male Balb/c mice exposed to intermittent hypobaric hypoxia (450 Torr; 4300 m) for 21 days and compared to normoxic (sea level) controls. In the hypoxic we found a 47% reduction of oxygen uptake during state 3 (ADP and substrate present), 12% reduction during state 4 (no ADP present) and 20% reduction in the uncoupled respiration rate with pyruvate plus malate as substrates. Respiratory control ratio (RCR) decreased by 24%. No change in the ADP/O ratio was seen. NADH CoQ reductase activity decreased by 30% and cytochrome c oxidase by 17%, suggesting that under conditions of chronic hypoxia, the reductions of mitochondrial respiratory activities are caused, at least in part, by enzymatic alterations of the electron transport chain (complex I and complex IV). The decreased activity of these enzymes could contribute to alterations in neuronal activity by reducing brain energy metabolism during development under conditions of chronic hypoxia.
在从暴露于间歇性低压缺氧（450托；4300米）21天的雄性Balb/c小鼠大脑皮层分离出的游离（非突触体）线粒体中，测量了呼吸活性以及NADH辅酶Q还原酶（复合体I）和细胞色素c氧化酶（复合体IV）的活性，并与常氧（海平面）对照组进行了比较。在缺氧组中，我们发现状态3（存在ADP和底物）期间氧气摄取减少了47%，状态4（不存在ADP）期间减少了12%，以丙酮酸加苹果酸作为底物时的解偶联呼吸速率降低了20%。呼吸控制率（RCR）下降了24%。ADP/O比值未见变化。NADH辅酶Q还原酶活性下降了30%，细胞色素c氧化酶下降了17%，这表明在慢性缺氧条件下，线粒体呼吸活性的降低至少部分是由电子传递链（复合体I和复合体IV）的酶促改变引起的。这些酶活性的降低可能通过在慢性缺氧条件下发育过程中降低脑能量代谢而导致神经元活动的改变。
