Kulinskiĭ V I, Vorob'eva L M
Biull Eksp Biol Med. 1978 Mar;85(3):291-4.
cAMP 10(-6) activates the liver mitochondria respiration in all the metabolic states and failed to change or increased the phosphorylation rate in the oxidation of saturating concentration of succinate and isocitrate. Preincubation of mitochondria or homogenate of the liver with cAMP is obligatory for this effect. The fraction V of serum albumin and EDTA did not prevent the effect. Noradrenaline enhanced the mitochondrial respiration only in incubation with the homogenate. The effect of noradrenaline and cAMP was not summed up. Probably the noradrenaline effect was mediated through cAMP. The data obtained are against the decisive role of the respiration and phosphorylation uncoupling or the oxidation substrate accumulation and lead to the assumption on the mitochondria enzymes activation.
环磷酸腺苷(cAMP)10⁻⁶在所有代谢状态下均可激活肝脏线粒体呼吸,且在琥珀酸和异柠檬酸饱和浓度氧化时,未能改变或提高磷酸化速率。线粒体或肝脏匀浆与cAMP预孵育是产生此效应的必要条件。血清白蛋白和乙二胺四乙酸(EDTA)的V组分并未阻止该效应。去甲肾上腺素仅在与匀浆孵育时增强线粒体呼吸。去甲肾上腺素和cAMP的效应未叠加。可能去甲肾上腺素的效应是通过cAMP介导的。所获数据与呼吸和磷酸化解偶联或氧化底物积累的决定性作用相悖,并导致关于线粒体酶激活的假设。