Lutz W H, Geisbuhler T P, Pollack J D, McClung H J, Merola A J
Biochem Med. 1985 Aug;34(1):1-10. doi: 10.1016/0006-2944(85)90055-9.
Liver mitochondria from octanoate-treated rabbits showed an impaired ability to synthesize citrulline. Two methods were used to evaluate citrulline synthesis in rat liver mitochondria. Under these conditions octanoate inhibited citrulline synthesis by over 50%. When ATP was included in the assay medium the inhibitory effect of octanoate was prevented. In the absence of ATP in the suspending medium, octanoate did not significantly lower total adenine nucleotides in rat liver mitochondria. However, under these conditions octanoate caused a change in the adenine nucleotide profile such that ATP content was decreased and AMP content was increased. When ATP was present in the assay medium, octanoate caused a similar increase in AMP content. However, ATP decreased only slightly. The alterations in mitochondrial adenine nucleotide profile by octanoate and the reversal of the effect by exogenous ATP suggests that octanoate inhibits citrulline synthesis via reduced intramitochondrial ATP levels. The ability of octanoate to lower mitochondrial ATP and elevate mitochondrial AMP may be related to its intramitochondrial activation by the medium chain fatty acid activating enzyme.
用辛酸处理过的兔子的肝脏线粒体显示出合成瓜氨酸的能力受损。使用了两种方法来评估大鼠肝脏线粒体中的瓜氨酸合成。在这些条件下,辛酸抑制瓜氨酸合成超过50%。当测定介质中包含ATP时,辛酸的抑制作用被阻止。在悬浮介质中不存在ATP的情况下,辛酸不会显著降低大鼠肝脏线粒体中的总腺嘌呤核苷酸。然而,在这些条件下,辛酸导致腺嘌呤核苷酸谱发生变化,使得ATP含量降低而AMP含量增加。当测定介质中存在ATP时,辛酸导致AMP含量出现类似增加。然而,ATP仅略有下降。辛酸引起的线粒体腺嘌呤核苷酸谱的改变以及外源性ATP对该作用的逆转表明,辛酸通过降低线粒体内ATP水平来抑制瓜氨酸合成。辛酸降低线粒体ATP并升高线粒体AMP的能力可能与其被中链脂肪酸活化酶在线粒体内激活有关。