Halperin M L, Robinson B H, Fritz I B
Proc Natl Acad Sci U S A. 1972 Apr;69(4):1003-7. doi: 10.1073/pnas.69.4.1003.
Palmitoyl CoA inhibited citrate transport from isolated rat liver mitochondria. Under conditions described, 50% inhibition was observed at about 6-8 nmol/mg of mitochondrial protein per ml. The percentage inhibition was inversely proportional to the concentration of the counter-transporting anion in the medium. Although comparable levels of palmitoyl CoA had little effect on malate exit on the dicarboxylate carrier, higher concentrations inhibited both citrate and malate transport. The specificity of the inhibition by palmitoyl CoA was investigated by examination of the effects on the tricarboxylate transport system of fatty acids, CoASH, acetyl CoA, palmitoylcarnitine, deoxycholate, and other molecules with surface active properties. None of the above compounds, at sublytic concentrations, inhibited citrate transport appreciably. The inhibition of citrate transport by low concentrations of palmitoyl CoA was rapid and could be prevented or partially reversed by addition of albumin.
棕榈酰辅酶A抑制了从分离的大鼠肝线粒体中柠檬酸的转运。在所述条件下,每毫升线粒体蛋白约6 - 8纳摩尔时观察到50%的抑制作用。抑制百分比与培养基中反向转运阴离子的浓度成反比。尽管相当水平的棕榈酰辅酶A对二羧酸载体上苹果酸的流出影响很小,但较高浓度会抑制柠檬酸和苹果酸的转运。通过研究脂肪酸、辅酶A、乙酰辅酶A、棕榈酰肉碱、脱氧胆酸盐和其他具有表面活性特性的分子对三羧酸转运系统的影响,来探究棕榈酰辅酶A抑制作用的特异性。在亚裂解浓度下,上述化合物均未明显抑制柠檬酸转运。低浓度的棕榈酰辅酶A对柠檬酸转运的抑制作用迅速,加入白蛋白可阻止或部分逆转这种抑制作用。