Verbunt R J, Van der Laarse A
Department of Cardiology, University Hospital, Leiden, The Netherlands.
Mol Cell Biochem. 1997 Feb;167(1-2):127-34. doi: 10.1023/a:1006821220600.
The objective of the present study was to determine whether mild ischemia hampers the use of tissue concentration of glutathione disulfide (GSSG) and release of GSSG as indices of oxidative stress in postischemic hearts. To this end, the response of the glutathione redox cycle to the prooxidant cumene hydroperoxide (CumOOH) was compared in non-ischemic and postischemic rat hearts perfused in vitro. Perfusion of non-ischemic and postischemic hearts with CumOOH (20-25 microM) for 10 min followed by 20 min of perfusion without CumOOH resulted in similar changes in tissue concentration of GSSG, and similar patterns of GSSG release. The similar response in tissue concentration of GSSG is consistent with the finding that mild ischemia did not affect the formation and reduction of GSSG. While release of GSSG from non-ischemic hearts was solely due to active transport of GSSG, release of GSSG from postischemic hearts was due to both active transport of GSSG and aspecific leakage of GSSG. In conclusion, tissue concentration of GSSG can be reliably used to investigate oxidative stress in postischemic hearts. However, the occurrence of aspecific leakage of GSSG, which is not indicative of oxidative stress, renders release of GSSG from postischemic hearts an unreliable index of oxidative stress.
本研究的目的是确定轻度缺血是否会妨碍将谷胱甘肽二硫化物（GSSG）的组织浓度和GSSG的释放用作缺血后心脏氧化应激指标。为此，在体外灌注的非缺血和缺血后大鼠心脏中，比较了谷胱甘肽氧化还原循环对促氧化剂氢过氧化异丙苯（CumOOH）的反应。用CumOOH（20 - 25 microM）灌注非缺血和缺血后心脏10分钟，然后在无CumOOH的情况下灌注20分钟，导致GSSG的组织浓度出现相似变化，以及GSSG释放的相似模式。GSSG组织浓度的相似反应与轻度缺血不影响GSSG的形成和还原这一发现一致。虽然非缺血心脏中GSSG的释放 solely 是由于GSSG的主动转运，但缺血后心脏中GSSG的释放是由于GSSG的主动转运和GSSG的非特异性泄漏。总之，GSSG的组织浓度可可靠地用于研究缺血后心脏的氧化应激。然而，GSSG的非特异性泄漏的发生并非氧化应激的指示，这使得缺血后心脏中GSSG的释放成为氧化应激的不可靠指标。
原文中“solely”一词翻译时漏了，已补充完整。
