Abstract

Moderate artificial hypothermia is widely used in clinical practice to protect organs from the effects of ischemia (reperfusion), trauma, and hypoxia. However, a decrease in the body temperature of homeothermic animals induces oxidative stress, the severity of which may depend on the time of exposure to the cold factor. Since mitochondria play a key role in the generation of reactive oxygen species, we studied the dependence of the intensity of free radical processes in rat liver mitochondria on the duration of moderate hypothermia (30°C). It turned out that short-term (30 min) hypothermia activates the processes of lipid peroxidation (POL), while the concentration of lipid hydroperoxides, Schiff bases, and malondialdehyde significantly increases. Prolongation of hypothermia to 1 h reduces the content of many lipid peroxidation products, and their normalization is observed with 3-h hypothermia. Short-term hypothermia and its prolongation up to 1 h is accompanied by oxidative destruction of mitochondrial proteins, which is manifested in a decrease in the content of sulfhydryl groups in them and an increase in carbonyl groups. At the same time, 3-h hypothermia contributes to the normalization of the studied markers of protein oxidative modification. The dynamics of changes in the levels of sulfhydryl and carbonyl groups in the mitochondrial matrix proteins is more pronounced in comparison with membrane proteins. The study of the spectral characteristics of mitochondrial membrane proteins showed a decrease in the intensity of their fluorescence at the initial stages of hypothermia. Tryptophan residues localized at the periphery make the main contribution to it. Prolongation of hypothermia up to 3 h contributes to restoration of fluorescence parameters to the control level. The data obtained in the analysis of the second derivative fluorescence spectra indicate changes in the spatial configuration of membrane proteins.

中文翻译：

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在不同持续时间的中等低温下大鼠肝线粒体的自由基过程强度

摘要

中等程度的人工低温在临床实践中被广泛使用，以保护器官免受缺血（再灌注），创伤和缺氧的影响。但是，等温动物的体温下降会引起氧化应激，其严重性可能取决于暴露于寒冷因素的时间。由于线粒体在活性氧的产生中起着关键作用，因此我们研究了大鼠肝脏线粒体中自由基过程的强度对中度低温（30°C）持续时间的依赖性。事实证明，短期（30分钟）体温过低会激活脂质过氧化（POL）过程，而脂质氢过氧化物，席夫碱和丙二醛的浓度会明显增加。将体温过低延长至1小时会减少许多脂质过氧化产物的含量，并在3小时低温下观察到它们的正常化。短期体温过低和延长至1 h会伴随着线粒体蛋白质的氧化破坏，这表现为线粒体蛋白质中巯基含量的减少和羰基含量的增加。同时，3 h低温有助于蛋白质氧化修饰修饰标记的标准化。与膜蛋白相比，线粒体基质蛋白中巯基和羰基水平的变化动态更为明显。线粒体膜蛋白的光谱特征研究表明，在体温过低的初期，其荧光强度降低。位于外围的色氨酸残基对此起主要作用。亚低温延长至3小时有助于将荧光参数恢复至对照水平。在二阶导数荧光光谱分析中获得的数据表明膜蛋白的空间构型发生变化。