McMurray W C
Can J Biochem. 1975 Jul;53(7):784-95. doi: 10.1139/o75-106.
When isolated mitochondria or microsomes from rat liver were treated with phospholipase C, the incorporation of radioactive phospholipid precursors was markedly enhanced, presumably as a result of production of diglycerides by hydrolysis of endogenous phospholipids. Incorporation of CDP[14C]choline into lecithin in rat liver or BHK-21 mitochondria could be attributed to residual contamination from elements of the endoplasmic reticulum, with added diglycerides or with endogenous diglycerides produced by the phospholipase C treatment. A similar stimulation of [gamma32P]ATP incorporation into phospholipids was observed with exogenous or endogenous diglycerides, but the mitochondrial diglyceride kinase in either case was also related to the degree of microsomal contaminants. It was concluded that previous studies showing negligible capacity of mitochondria for lecithin biosynthesis de novo were not explainable on the basis of limited accessibility of added diglycerides, and that formation of phosphatidic acid by diglyceride kinase was not of significance in rat liver mitochondria.
当用磷脂酶C处理大鼠肝脏分离出的线粒体或微粒体时,放射性磷脂前体的掺入显著增强,这可能是由于内源性磷脂水解产生甘油二酯的结果。在大鼠肝脏或BHK - 21线粒体中,CDP[14C]胆碱掺入卵磷脂可归因于内质网成分的残留污染,添加甘油二酯或磷脂酶C处理产生的内源性甘油二酯也会导致这种情况。用外源性或内源性甘油二酯时,观察到[γ32P]ATP掺入磷脂有类似的刺激作用,但在这两种情况下,线粒体甘油二酯激酶也与微粒体污染物的程度有关。得出的结论是,先前显示线粒体从头合成卵磷脂能力可忽略不计的研究,不能基于添加甘油二酯的有限可及性来解释,并且甘油二酯激酶形成磷脂酸在大鼠肝脏线粒体中并不重要。