The role of mitochondria in oxidative and nitrosative stress during ischemia/reperfusion in the rat kidney

被引：171

作者：

Plotnikov, E. Y.

Kazachenko, A. V.

Vyssokikh, M. Y.

Vasileva, A. K.

Tcvirkun, D. V.

Isaev, N. K.

Kirpatovsky, V. I.

Zorov, D. B. ^{[1
]}

机构：

[1] Moscow MV Lomonosov State Univ, AN Belozerky Inst Physico Chem Biol, Lab Mitochondrial Struct & Funct, Moscow 119992, Russia

[2] Mitotechnol LLC, Moscow, Russia

[3] Minist Publ Hlth Russia, Res Inst Urol, Moscow, Russia

[4] Moscow MV Lomonosov State Univ, Fac Biol, Moscow 119992, Russia

来源：

KIDNEY INTERNATIONAL | 2007年 / 72卷 / 12期

基金：

俄罗斯基础研究基金会;

关键词：

ischemia; mitochondria; reactive oxygen species; preconditioning; kidney;

D O I：

10.1038/sj.ki.5002568

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

Reoxygenation following ischemia causes tissue oxidative stress. We studied the role of oxidative stress caused by kidney ischemia/reperfusion (I/R) on the mitochondria of renal tissue slices. I/R caused the mitochondria to be swollen, fragmented, and have lower membrane potential. The mitochondria generated more reactive oxygen species (ROS) and nitric oxide (NO) in situ as measured by fluorescence of ROS- and NO-sensitive probes. Infusion of lithium ion, an inhibitor of glycogen kinase synthase-3, caused phosphorylation of its Ser-9 and restored the membrane potential and decreased ROS production of the mitochondrial fraction. Ischemic kidney and hypoxic rat preconditioning improved mitochondrial membrane potential and lowered ROS production caused by subsequent I/R similar to lithium ion infusion. Preconditioning normalized NO production in mitochondria as well. The drop in the mitochondrial membrane potential was prevented by NO synthase inhibition, demonstrating a strong contribution of NO to changes in mitochondrial energy metabolism during the I/R transition. Mitochondria in the I/R-stressed kidney contained less cytochrome c and more pro-apoptotic Bax, consistent with apoptotic degradation.

引用

页码：1493 / 1502

页数：10

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