HYDROXYL RADICAL GENERATION BY POSTISCHEMIC RAT-KIDNEY SLICES INVITRO

被引：17

作者：

STEINER, MG ^{[1
]}

BABBS, CF ^{[1
]}

机构：

[1] PURDUE UNIV,DEPT VET PHYSIOL & PHARMACOL,W LAFAYETTE,IN 47907

来源：

FREE RADICAL BIOLOGY AND MEDICINE | 1990年 / 9卷 / 01期

关键词：

Fenton Reaction; Free Radical; Hydroxyl radical; Kidney; Reperfusion injury; Superoxide radical;

D O I：

10.1016/0891-5849(90)90051-J

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

To quantitate the formation of hydroxyl radicals (HO·) in ischemia and reoxygenation, dimethyl sulfoxide (DMSO) was added to "trap" evolving HO· in normal, in ischemic, and in schemic and reoxygenated rat kidney slices, incubated in short-term organ culture in vitro. Hydroxyl radical generation was measured as the accumulation of the specific product of DMSO oxidation by HO·, methane sulfinic acid (MSA) in the kidney tissue and surrounding medium using a new colorimetric assay. A mean difference of 7 nmol cumulative HO·/gram tissue was detected in rat kidney slices subjected to ischemia and reoxygenation. This amount of HO· generation was not significantly greater than that found in nonischemic or in schemic but not reoxygenated control tissues, and does not appear to represent the higly toxic burst of HO· radicals implied in current theoretical discussions of reperfusion injury. However, the addition of EDTA chelated iron (1:1) to the incubation medium led to marked postischemic HO· generation. We conclude that clearly toxic numbers of HO· radicals are not formed during reoxygenation in rat kidney slices, either because there is insufficient iron, because only a small fraction of cells in the kidney tissue make oxygen radicals, or because cellular defenses against HO· formation are more powerful than currently appreciated. © 1990.

引用

页码：67 / 77

页数：11

共 71 条

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