微摩尔浓度的钙可防止离体大鼠肝线粒体发生缺氧-复氧损伤。

Micromolar calcium prevents isolated rat liver mitochondria from anoxia-reoxygenation injury.

作者信息

Schild L, Plumeyer F, Reinheckel T, Augustin W

机构信息

Department of Pathobiochemistry, Otto-von-Guericke-University, Medical Faculty, Magdeburg, Germany.

出版信息

Biochem Mol Biol Int. 1997 Sep;43(1):35-45. doi: 10.1080/15216549700203791.

DOI:10.1080/15216549700203791

PMID:9315280

Abstract

Rat liver mitochondria were exposed to extramitochondrial free calcium between 0 and 5 microM and/or 5 minutes of anoxia followed by 10 minutes of reoxygenation. At concentrations higher than 4 microM, the membrane potential collapsed indicating the permeability transition of the mitochondrial membrane. Anoxia-reoxygenation shifted this transition to lower calcium concentrations. Anoxia-reoxygenation alone resulted in the decrease of ADP stimulated respiration down to about 40% of its initial value. Between 1 and 2 microM, a protective effect in terms of respiration and oxidative protein modification was found. It is concluded that calcium may suppress the formation of reactive oxygen species during anoxia-reoxygenation before permeability transition occurs.

摘要

将大鼠肝脏线粒体暴露于0至5微摩尔的线粒体外游离钙中，和/或进行5分钟缺氧，随后再进行10分钟复氧。当浓度高于4微摩尔时，膜电位崩溃，表明线粒体膜发生通透性转变。缺氧-复氧将这种转变转移至更低的钙浓度。单独的缺氧-复氧导致ADP刺激的呼吸作用下降至其初始值的约40%。在1至2微摩尔之间，发现了对呼吸作用和氧化蛋白质修饰的保护作用。得出的结论是，在通透性转变发生之前，钙可能会抑制缺氧-复氧期间活性氧的形成。