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缺血再灌注损伤对过氧化物酶体形态的影响。

Effect of ischemia-reperfusion injury on the morphology of peroxisomes.

作者信息

Singh A K, Gulati S

机构信息

Department of Pathology, Ralph H. Johnson V.A. Medical Center, Charleston, S.C. 29401, USA.

出版信息

Mol Cell Biochem. 1995 Mar 9;144(1):19-26. doi: 10.1007/BF00926736.

Abstract

We have previously demonstrated that ischemic injury changed the density of peroxisomes into two distinct peaks, one with a normal density (1.21 g/cm3; Peak I) and a second peak with a lighter density (1.14 g/cm3; Peak II). We studied the peroxisomes from both peaks under the Electron microscope. Examination of peak I following ischemia showed loss of matrix proteins and damaged limiting membranes with leakage of DAB positive material in direct proportion to the duration of ischemia. Upon reperfusion of the ischemic liver Peak I showed more severe damage to the organelle. These observations clearly demonstrated that ischemia reperfusion injury causes structural damage to peroxisomes. Interestingly ultrastructural examination of Peak II following ischemia showed evidence of perisomal proliferation with budding of existing peroxisomes and the presence of micro peroxisomes (changes similar to those noted under conditions leading to perisomal proliferation). However, peak II following reperfusion showed only damaged organelle. These observations underline the importance of peroxisomes in the response of the cell to ischemia-reperfusion injury.

摘要

我们之前已经证明,缺血性损伤会使过氧化物酶体的密度变为两个不同的峰值,一个具有正常密度(1.21 g/cm³;峰I),另一个峰值密度较轻(1.14 g/cm³;峰II)。我们在电子显微镜下研究了这两个峰值的过氧化物酶体。对缺血后的峰I进行检查发现,基质蛋白丢失,限制膜受损,DAB阳性物质泄漏,且与缺血持续时间成正比。缺血肝脏再灌注后,峰I对细胞器的损伤更严重。这些观察结果清楚地表明,缺血再灌注损伤会导致过氧化物酶体的结构损伤。有趣的是,对缺血后的峰II进行超微结构检查发现,存在过氧化物酶体增殖的迹象,现有过氧化物酶体出芽,并且存在微过氧化物酶体(这些变化与在导致过氧化物酶体增殖的条件下观察到的变化相似)。然而,再灌注后的峰II仅显示细胞器受损。这些观察结果强调了过氧化物酶体在细胞对缺血再灌注损伤反应中的重要性。

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