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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Glutathione monoethylester prevents mitochondrial glutathione depletion during focal cerebral ischemia.
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Glutathione monoethylester prevents mitochondrial glutathione depletion during focal cerebral ischemia.

机译：谷胱甘肽单乙酯可防止局灶性脑缺血期间线粒体谷胱甘肽耗竭。

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摘要

Glutathione is a central component in the antioxidant defences of cells. We have recently reported an early and selective loss of total (reduced plus oxidised) glutathione from mitochondria isolated from rat brain following occlusion of the middle cerebral artery. This mitochondrial glutathione depletion showed an apparent association with the tissue damage that developed during subsequent reperfusion, suggesting that it could be an important determinant of susceptibility to cell loss. In the present study, we have investigated whether in vivo treatment with glutathione ethyl ester can modulate mitochondrial glutathione in the brain and whether this treatment can influence the response to focal ischemia. In further support of our previous findings, middle cerebral artery occlusion caused a duration-dependent partial loss of mitochondrial glutathione. Bilateral injections of glutathione ethyl ester immediately prior to induction of unilateral focal ischemia resulted in a substantial increase in glutathione in mitochondria from the striatum of both the non-ischemic hemisphere (190% of saline-treated controls) and the ischemic hemisphere (240% of controls) at 2h after arterial occlusion. Total tissue glutathione was not affected by the ester treatment at this time. A smaller increase in mitochondrial glutathione was observed at 3h of occlusion in the non-ischemic striatum following ester treatment but at this time point glutathione was not significantly altered in mitochondria from the ischemic hemisphere. Pre-ischemic treatment with glutathione ester did not significantly change the volume of tissue infarction assessed at 48 h following ischemia for 2 or 3h. These studies demonstrate that glutathione ethyl ester is a highly effective modulator of the mitochondrial glutathione pool in the intact brain and provides a useful means for further investigating the role of this antioxidant in the development of tissue damage in ischemia and other brain disorders.
机译：谷胱甘肽是细胞抗氧化防御的重要组成部分。最近，我们报道了大脑中动脉闭塞后，从大鼠脑中分离出的线粒体中的谷胱甘肽总量（还原型和氧化型）的早期选择性丧失。线粒体谷胱甘肽耗竭表明与随后的再灌注过程中发生的组织损伤明显相关，这表明它可能是细胞丢失易感性的重要决定因素。在本研究中，我们调查了体内谷胱甘肽乙酯治疗是否可以调节脑线粒体谷胱甘肽，以及这种治疗是否可以影响对局灶性局部缺血的反应。为了进一步支持我们先前的发现，大脑中动脉闭塞导致线粒体谷胱甘肽持续时间依赖性部分丢失。刚诱导单侧局灶性局部缺血之前，双边注射谷胱甘肽乙酯会导致线粒体中非缺血性半球（盐水处理过的对照组的190％）和缺血性半球的纹状体中谷胱甘肽的大量增加。对照）在动脉闭塞后2小时。此时总组织谷胱甘肽不受酯处理的影响。酯处理后，非缺血性纹状体在闭塞3h时线粒体谷胱甘肽的增加较小，但此时线粒体中的谷胱甘肽没有明显改变，来自缺血半球。用谷胱甘肽酯进行缺血前治疗并没有显着改变在缺血后2小时或3小时48小时评估的组织梗死的体积。这些研究表明，谷胱甘肽乙酯是完整大脑中线粒体谷胱甘肽池的高效调节剂，并为进一步研究这种抗氧化剂在缺血和其他脑部疾病的组织损伤发展中的作用提供了有用的手段。

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