Kurhaliuk N M
Ivan Franko Lviv National University.
Fiziol Zh (1994). 2001;47(3):64-72.
In experiments on rats with different resistance to hypoxia are investigated processes of mitochondrial respiration, oxidative phosphorylation and calcium capacity in liver under precursor nitric oxide L-arginine (600 mg/kg) and blockator nitric oxide synthase L-NNA (35 mg/kg) injections. We are used next substrates of oxidation: 0.35 mM succinate, 1 mM alpha-ketoglutarate, 1 mM alpha-ketoglutarate and 2 mM malonic acid. Increasing of ADP-stimulation respiration states under exogenous L-arginine injection, decreasing efficacy of respiration processes (respiration control on Chance and ADP/O) under such substrates oxidation, testify to oxide energy support decreasing and reversing nitric oxide inhibit in such conditions. This will be used as mechanism cell regulation succinate dehydrogenase activity. It has shown that L-arginine injection increase calcium mitochondrial capacity low resistance to hypoxia rats using substrates of oxidation succinate and alpha-ketoglutarate to control meanings of high resistance rats. Effects of nitric oxide precursor influence on this processes limit NO-synthase inhibitor L-NNA.
在对不同缺氧耐受性大鼠的实验中，研究了在注射一氧化氮前体L-精氨酸（600毫克/千克）和一氧化氮合酶阻断剂L-NNA（35毫克/千克）后，肝脏中线粒体呼吸、氧化磷酸化和钙容量的变化过程。我们使用了以下氧化底物：0.35毫摩尔琥珀酸、1毫摩尔α-酮戊二酸、1毫摩尔α-酮戊二酸和2毫摩尔丙二酸。外源性L-精氨酸注射后ADP刺激呼吸状态增加，在这些底物氧化时呼吸过程的效率降低（根据Chance法和ADP/O进行呼吸控制），这证明在这种情况下氧化能量支持减少且一氧化氮抑制作用逆转。这将被用作细胞调节琥珀酸脱氢酶活性的机制。结果表明，注射L-精氨酸可增加低缺氧耐受性大鼠使用琥珀酸和α-酮戊二酸氧化底物时的线粒体钙容量，使其达到高耐受性大鼠的对照水平。一氧化氮前体对这些过程的影响受到一氧化氮合酶抑制剂L-NNA的限制。
