Ellerbe P, Murphy R B, Rose H G
Chem Phys Lipids. 1985 Sep;38(3):275-85. doi: 10.1016/0009-3084(85)90021-0.
The regulation of human plasma lecithin:cholesterol acyltransferase (LCAT) by changes in bilayer fluidity of substrate egg phosphatidylcholine (egg PC) unilamellar vesicles was investigated using pyrene excimer fluorescence to measure fluidity. Fluidity was decreased by adding up to 20% cholesterol or increased by adding up to 10% egg 2-lysophosphatidylcholine (lysoPC). The fluidizing effect of lysoPC was suppressed by the addition of cholesterol. LCAT activity with 10% cholesterol vesicles was decreased by adding 5% lysoPC, yet activity with 5% cholesterol vesicles was unaffected by adding 5% lysoPC. This difference may be explained by a balance between the known LCAT inhibitory effect of lysoPC and its ability to increase bilayer fluidity and thereby increase LCAT activity. LCAT esterification of up to 37% of vesicle cholesterol failed to alter the lysoPC/cholesterol balance sufficiently to influence activity in this system. The findings of our studies are in keeping with modulation of LCAT activity by bilayer fluidity, but fluidity changes caused by enzyme action are not sufficient to regulate that activity.
利用芘激基荧光测量流动性，研究了底物卵磷脂酰胆碱（卵PC）单层囊泡的双层流动性变化对人血浆卵磷脂：胆固醇酰基转移酶（LCAT）的调节作用。通过添加高达20%的胆固醇可降低流动性，或通过添加高达10%的卵2-溶血磷脂酰胆碱（溶血PC）来增加流动性。胆固醇的添加抑制了溶血PC的流化作用。添加5%溶血PC可使含10%胆固醇囊泡的LCAT活性降低，但添加5%溶血PC对含5%胆固醇囊泡的活性没有影响。这种差异可能是由于溶血PC已知的LCAT抑制作用与其增加双层流动性从而增加LCAT活性的能力之间的平衡所致。高达37%的囊泡胆固醇的LCAT酯化作用未能充分改变溶血PC/胆固醇平衡，从而影响该系统中的活性。我们的研究结果表明LCAT活性受双层流动性调节，但酶作用引起的流动性变化不足以调节该活性。
