Effects of oxidative stress on the expression of antioxidative defense enzymes in spontaneously hypertensive rat hearts
Effects of oxidative stress on the expression of antioxidative defense enzymes in spontaneously hypertensive rat hearts
复制标题
DOI：
10.1016/s0891-5849(00)00365-8
复制
发表时间：
2000-10-01
影响因子：
7.4
通讯作者：
Blasig, IE
中科院分区：
文献类型：
--
作者：
Csonka, C;Pataki, T;Blasig, IE
自发性高血压大鼠(SHR)是一种扩张型心肌病模型，其失代偿心肌肥厚过程中氧化应激对抗氧化酶表达的影响尚不清楚。在18月龄自发性高血压大鼠(SHR)和年龄匹配的正常血压对照组(WKY)大鼠心脏灌流前和灌流30min后，分别测定了超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPX)的活性。注入H_2O_2后，WKY组的主动脉流量从26.2±2.2降至16.0±0.8毫升/分(p<；0.05)，而SHR则无明显变化(18.2±1.9比20.7±2.2毫升/分)。与WKY组相比，SHR大鼠心肌组织中的GPX、MnSOD和CuZnSOD活性明显升高，提示这种保护作用可能与其对心肌的保护作用有关。尽管如此。与输注前相比，H2O暴露后SHR的总SOD活性下降(从3.56 U/mg蛋白降至1.81+/-0.13 U/mg蛋白)，过氧化氢酶活性升高(从1.56+/-0.29 k min(-1)mg(-1)蛋白上升至2.46+/-0.34蛋白)(p<；0.05)。在另外的研究中，心脏经历了30分钟的全脑缺血和30分钟的再灌流。在缺血/再灌流心脏中测得的酶活性变化与在过氧化氢灌流心脏中观察到的变化相同，表明氧化应激与其诱导的方式无关。较高的过氧化氢酶活性来自于较高的mRNA合成。在失代偿过程中，SHR扩张型心肌病心脏的抗氧化系统被诱导，可能是由于氧化应激事件。这种对抗氧化能力的调节可能有助于克服衰竭心肌中活性氧物种引起的急性应激情况。(C)2000年爱思唯尔科学公司。
Little is known concerning the effect of oxidative stress on the expression of antioxidative enzymes in the decompensated cardiac hypertrophy of spontaneously hypertensive rats (SHR), considered as a model of dilative cardiomyopathy in man. Superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) were characterized in isolated perfused hearts of 18 month old SHR and the age-matched normotensive control Wistar-Kyoto (WKY) rats, before and after 30 min infusion of 25 muM H2O2. After infusion of H2O2, aortic flow decreased in WKY from 26.2 +/- 2.2 to 16.0 +/- 0.8 mlmin (p < .05) but not in SHR (18.2 +/- 1.9 vs. 20.7 +/- 2.2 ml/min). This protection was related to the higher myocardial activities of GPx, MnSOD and CuZnSOD in SHR, compared with those of the WKY group. Although. total SOD activity in the SHR fell after H2O2 exposure (to 1.81 +/- 0.13 from 3.56 to 0.49 U/mg of protein), catalase activity increased (to 2.46 +/- 0.34 from 1.56 +/- 0.29 k min(-1)mg(-1)protein), compared with the pre-infusion period (p < .05 in each case). In additional studies, hearts were subjected to 30 min of global ischemia followed by 30 min of reperfusion. The results obtained in ischemic/reperfused hearts show the same changes in enzyme activities measured as it was observed in H2O2 perfused hearts, indicating that oxidative stress is independent of the way it was induced. The higher catalase activity derived from elevated mRNA synthesis. The antioxidative system in dilative cardiomyopathic hearts of SHR is induced, probably due to episodes of oxidative stress, during the process of decompensation. This conditioning of the antioxidative potential may help overcome acute stress situations caused by reactive oxygen species in the failing myocardium. (C) 2000 Elsevier Science Inc.