Okuda M, Lee H C, Wu Q Y, Chance B, Kumar C
Department of Biochemistry and Biophysics, University of Pennsylvania School of Medicine, Philadelphia 19104-6089.
Res Commun Chem Pathol Pharmacol. 1992 Oct;78(1):17-25.
Perfusion of rat liver with Ca(2+)-depleted buffer induces oxidative stress and liver damage, which can be prevented by Ca2+ repletion (Okuda et al. J Lab Clin Med). In the present study, we investigated the action of ruthenium red on acute Ca2+ loading after Ca2+ depletion in the isolated perfused rat liver. The major findings of this study are that 1) Ca2+ depletion-induced liver damage was related to mitochondrial disfunction; 2) ruthenium red inhibited the oxidative stress and liver damage normally seen during Ca2+ depletion; 3) ruthenium red inhibited the Ca2+ depletion-induced mitochondrial disfunction. These observations suggest that mitochondrial Ca2+ cycling is responsible for Ca2+ depletion-induced oxidative stress and liver damage.
用缺钙缓冲液灌注大鼠肝脏会引发氧化应激和肝损伤,而补充钙离子可预防这种情况(奥田等人,《实验与临床医学杂志》)。在本研究中,我们调查了钌红对离体灌注大鼠肝脏缺钙后急性钙负荷的作用。本研究的主要发现是:1)缺钙诱导的肝损伤与线粒体功能障碍有关;2)钌红抑制了缺钙期间通常出现的氧化应激和肝损伤;3)钌红抑制了缺钙诱导的线粒体功能障碍。这些观察结果表明,线粒体钙循环是缺钙诱导的氧化应激和肝损伤的原因。