Janssen M, Koster J F, Bos E, de Jong J W
Thoraxcenter, Erasmus University Rotterdam, The Netherlands.
Circ Res. 1993 Oct;73(4):681-8. doi: 10.1161/01.res.73.4.681.
A number of studies show the relation between oxygen-derived free radicals and cardiac ischemia/reperfusion injury. However, little is known about oxidative stress in the human heart, which can be measured by oxidized glutathione (GSSG) and malondialdehyde (MDA) formation. Furthermore, data on MDA production by rat hearts are controversial, possibly because of the use of the aspecific thiobarbituric acid assay. Therefore, GSSG and MDA were measured, with colorimetric and high-performance liquid chromatographic assays, respectively, in buffer-perfused explanted human hearts and normal rat hearts made temporarily ischemic. Human hearts received cardioplegia; rat hearts were studied in a control and an ischemic group with or without cardioplegia. Baseline GSSG release was < 0.01 nmol.min-1.g wet wt-1 in both species. During reperfusion, GSSG release from human hearts and from ischemic and cardioplegic/ischemic rat hearts peaked at 0.24 +/- 0.12, 1.1 +/- 0.4, and 0.19 +/- 0.04 nmol.min-1.g-1, respectively. MDA was undetectable (< 0.02 nmol.min-1.g-1) in the effluent of both species and in human hearts (< 4 nmol/g protein). Rat heart reduced glutathione levels decreased 32% as a consequence of cardioplegia and ischemia. Cardioplegia induced a 41% (P = .08) decrease in rat heart MDA content, whereas cumene hydroperoxide increased it 3.6 times (P < .01). Thus, after ischemia human and rat hearts release GSSG, indicating that oxidative stress has occurred. Apparently, lipid peroxidation takes place in normal rat hearts, decreases after cardioplegia, but does not increase after ischemia/reperfusion. Human hearts lack MDA under normoxic and ischemic conditions. This novel finding seems to reflect a low MDA-forming potential in both situations.(ABSTRACT TRUNCATED AT 250 WORDS)
多项研究表明了氧衍生自由基与心脏缺血/再灌注损伤之间的关系。然而，对于可通过氧化型谷胱甘肽（GSSG）和丙二醛（MDA）生成来衡量的人体心脏氧化应激，人们了解甚少。此外，关于大鼠心脏MDA生成的数据存在争议，这可能是由于使用了非特异性硫代巴比妥酸检测法。因此，分别采用比色法和高效液相色谱法，对缓冲液灌注的离体人体心脏和造成暂时缺血的正常大鼠心脏中的GSSG和MDA进行了检测。人体心脏接受了心脏停搏液灌注；大鼠心脏在有或无心脏停搏液灌注的情况下分为对照组和缺血组进行研究。两种心脏的基线GSSG释放量均<0.01 nmol·min⁻¹·g湿重⁻¹。再灌注期间，人体心脏以及缺血和心脏停搏液灌注/缺血大鼠心脏的GSSG释放量分别在0.24±0.12、1.1±0.4和0.19±0.04 nmol·min⁻¹·g⁻¹时达到峰值。两种心脏流出液以及人体心脏中均未检测到MDA（<0.02 nmol·min⁻¹·g⁻¹和<4 nmol/g蛋白质）。心脏停搏液灌注和缺血导致大鼠心脏还原型谷胱甘肽水平降低32%。心脏停搏液灌注使大鼠心脏MDA含量降低了41%（P = 0.08），而异丙苯过氧化氢使其增加了3.6倍（P < 0.01）。因此，缺血后人体和大鼠心脏均释放GSSG，表明发生了氧化应激。显然，正常大鼠心脏中发生了脂质过氧化，心脏停搏液灌注后降低，但缺血/再灌注后未增加。在常氧和缺血条件下，人体心脏均缺乏MDA。这一新发现似乎反映了在这两种情况下MDA生成潜力较低。（摘要截选至250字）
