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对具有改变的磷脂去饱和酶活性的大鼠肝脏微粒体进行的荧光偏振研究。

Fluorescence polarization studies of rat liver microsomes with altered phospholipid desaturase activities.

作者信息

Pugh E L, Kates M, Szabo A G

出版信息

Can J Biochem. 1980 Oct;58(10):952-8. doi: 10.1139/o80-130.

DOI:10.1139/o80-130
PMID:7459688
Abstract

Phospholipid desaturase activity of rat liver microsomes can be varied by dietary manipulation: rats starved and refed a "fat-free" diet have two to three times the activity of normal controls whereas starved rats have no detectable activity. These changes were accompanied by changes in fatty acid composition of the microsomal phospholipids, resulting in a double bond: saturated fatty acid mole ratio (moles double bonds per mole saturated fatty acid) of 5.7 in control and starved rats and 4.7 in starved-refed rats. Fluorescence polarization ratio P (I parallel/I perpendicular to x instrument correction factor) of cis- and trans-parinaric acid (PnA) showed no significant differences in physical state of the three microsomal preparations. However, the isolated microsomal phospholipids with trans-PnA as probe showed differences in the temperature at which onset of a change in polarization ratio occurred (starved-refed greater than normal greater than starved rats). With the cis-PnA as probe, the polarization ratio showed no change in the range 10-40 degrees C but was significantly higher (1.8) in starved-refed rats than in normal and starved rats (1.6 in both cases). These data indicate that the microsomal phospholipids of starved-refed animals were in a less fluid state than those from control and starved rats and that this decrease in fluidity was correlated with an increase in phospholipid desaturase activity.

摘要

大鼠肝脏微粒体的磷脂去饱和酶活性可通过饮食调控而改变

饥饿后再喂食“无脂”饮食的大鼠,其活性是正常对照组的两到三倍,而饥饿大鼠则无可检测到的活性。这些变化伴随着微粒体磷脂脂肪酸组成的改变,导致对照组和饥饿大鼠的双键:饱和脂肪酸摩尔比(每摩尔饱和脂肪酸中的双键摩尔数)为5.7,饥饿后再喂食的大鼠为4.7。顺式和反式紫黄质酸(PnA)的荧光偏振比P(I平行/I垂直×仪器校正因子)在三种微粒体制剂的物理状态上没有显著差异。然而,以反式PnA为探针分离的微粒体磷脂在偏振比发生变化的起始温度上存在差异(饥饿后再喂食的大鼠>正常大鼠>饥饿大鼠)。以顺式PnA为探针时,偏振比在10 - 40℃范围内没有变化,但饥饿后再喂食的大鼠的偏振比(1.8)显著高于正常大鼠和饥饿大鼠(两者均为1.6)。这些数据表明,饥饿后再喂食的动物的微粒体磷脂比对照组和饥饿大鼠的微粒体磷脂处于流动性更低的状态,并且这种流动性的降低与磷脂去饱和酶活性的增加相关。

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