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通过在水性聚合物双相系统中的分配测定几种条件下大鼠肝脏过氧化物酶体膜表面性质的变化。

Changes in membrane surface properties of hepatic peroxisomes of rats under several conditions as determined by partition in aqueous polymer two-phase systems.

作者信息

Horie S, Ishii H, Orii H, Suga T

出版信息

Biochim Biophys Acta. 1982 Aug 25;690(1):74-80. doi: 10.1016/0005-2736(82)90240-1.

DOI:10.1016/0005-2736(82)90240-1
PMID:7126569
Abstract

Changes in membrane surface properties of hepatic peroxisomes of rats under several conditions were observed by aqueous polymer two-phase systems, which contained 6% (w/w) dextran T 500, 6% (w/w) polyethyleneglycol 4000, 250 mmol sucrose/kg and various concentrations of sodium phosphate buffer. The partition of peroxisomes into the upper phase depended to a large extent on their membrane surface charge. The cross-points of peroxisomes shifted from 5.55 to 5.25 and 5.2 after the administration of clofibrate and aspirin for 2 weeks, respectively, although that of alloxan-diabetic rat peroxisomes was not altered. The hydrophobic properties of peroxisomes, examined by means of a partition containing polyethyleneglycol monostearate, were altered by diabetes and starvation, but no change occurred in rats treated with clofibrate or aspirin. In the liver of rats fed a high-fat diet, the partition of peroxisomes was the same as that of the control. These findings indicate that hypolipidemic drugs such as clofibrate and aspirin induce the proliferation of peroxisomes and lead to the alteration of the surface charge of peroxisomal membranes. Diabetes or fasting lead to an alteration mainly of the hydrophobic properties. Both changes are probably due to alteration of content and/or composition of the proteins and the phospholipids in peroxisomal membrane under the conditions used.

摘要

采用含有6%(w/w)葡聚糖T 500、6%(w/w)聚乙二醇4000、250 mmol蔗糖/kg以及不同浓度磷酸钠缓冲液的水相聚合物双相系统,观察了几种条件下大鼠肝脏过氧化物酶体膜表面性质的变化。过氧化物酶体在上相中的分配在很大程度上取决于其膜表面电荷。分别给予氯贝丁酯和阿司匹林2周后,过氧化物酶体的交叉点分别从5.55移至5.25和5.2,而四氧嘧啶糖尿病大鼠过氧化物酶体的交叉点未改变。通过含有聚乙二醇单硬脂酸酯的分配来检测,过氧化物酶体的疏水性质因糖尿病和饥饿而改变,但用氯贝丁酯或阿司匹林治疗的大鼠未发生变化。在喂食高脂饮食的大鼠肝脏中,过氧化物酶体的分配与对照组相同。这些发现表明,氯贝丁酯和阿司匹林等降血脂药物可诱导过氧化物酶体增殖,并导致过氧化物酶体膜表面电荷的改变。糖尿病或禁食主要导致疏水性质的改变。这两种变化可能是由于在所使用的条件下,过氧化物酶体膜中蛋白质和磷脂的含量和/或组成发生了改变。

相似文献

1
Changes in membrane surface properties of hepatic peroxisomes of rats under several conditions as determined by partition in aqueous polymer two-phase systems.通过在水性聚合物双相系统中的分配测定几种条件下大鼠肝脏过氧化物酶体膜表面性质的变化。
Biochim Biophys Acta. 1982 Aug 25;690(1):74-80. doi: 10.1016/0005-2736(82)90240-1.
2
Isolation of peroxisomes from rat liver using sucrose and Percoll gradients.使用蔗糖和 Percoll 梯度从大鼠肝脏中分离过氧化物酶体。
J Biochem Biophys Methods. 1981 Oct;5(4):203-17. doi: 10.1016/0165-022x(81)90045-2.
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Matrical inclusions of peroxisomes induced by clofibrate in preneoplastic hepatocytes of rats fed 3'-methyl-4-dimethyl-aminoazobenzene.在喂食3'-甲基-4-二甲基氨基偶氮苯的大鼠的癌前肝细胞中,氯贝丁酯诱导的过氧化物酶体基质内含物。
Gan. 1982 Feb;73(1):7-13.
4
Freeze-fracture study of rat liver peroxisomes: evidence for an induction of intramembrane particles by agents stimulating peroxisomal proliferation.
Eur J Cell Biol. 1990 Dec;53(2):227-33.
5
Determination of the cross-points of rat liver peroxisomes, peroxisomal core and the core components by cross-partition.通过交叉分区确定大鼠肝脏过氧化物酶体、过氧化物酶体核心及核心成分的交叉点。
Biochim Biophys Acta. 1979 Jul 4;585(3):435-43. doi: 10.1016/0304-4165(79)90088-6.
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Polydispersity of rat liver peroxisomes induced by the hypolipidemic and carcinogenic agent clofibrate.降血脂及致癌剂氯贝丁酯诱导的大鼠肝脏过氧化物酶体的多分散性。
Eur J Cell Biol. 1981 Apr;24(1):62-9.
7
Studies on peroxisomes. V. Effect of ethyl p-chlorophenoxyisobutyrate on the centrifugal behavior of rat liver peroxisomes.过氧化物酶体的研究。V. 对氯苯氧异丁酸乙酯对大鼠肝脏过氧化物酶体离心行为的影响。
J Biochem. 1975 Jun;77(6):1199-204.
8
Protein organization in mouse liver peroxisomes.小鼠肝脏过氧化物酶体中的蛋白质组织
Arch Biochem Biophys. 1992 Feb 1;292(2):605-12. doi: 10.1016/0003-9861(92)90038-x.
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Changes in CoA pools in hepatic peroxisomes of the rat under various conditions.不同条件下大鼠肝脏过氧化物酶体中辅酶A池的变化。
J Biochem. 1986 May;99(5):1345-52. doi: 10.1093/oxfordjournals.jbchem.a135602.
10
31P-NMR of liver peroxisome membranes from normal and clofibrate-treated rats.
Cell Mol Biol (Noisy-le-grand). 1993 Jul;39(5):479-89.

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