Abstract —A rapid increase in the concentration of free radicals and reactive oxygen species at the reperfusion stage is the most dangerous stage of ischemia–reperfusion injury. An avalanche-like increase in the level of reactive oxygen species and secondary products of free radical oxidation of biological macromolecules leads to the development of oxidative stress. The use of exogenous antioxidants can reduce the concentration of reactive oxygen species in the affected tissues and suppress or correct the course of oxidative stress; thus, it significantly reduces the severity of ischemia–reperfusion injury. Acute ischemic renal failure is one of the most important social problems in a comprehensive list of pathologies associated with ischemia–reperfusion. The nephroprotective effect of a chimeric PSH antioxidant enzyme that includes human peroxiredoxin 6 and Mn-containing superoxide dismutase of Escherichia coli has been shown on an animal model of bilateral ischemia–reperfusion renal injury. The recombinant chimeric PSH protein was able to neutralize a maximally possible wide range of reactive oxygen species due to the superoxide dismutase and peroxidase activities. It has been shown with histological, biochemical, and molecular biological methods that the preliminary administration of the chimeric PSH protein before ischemia–reperfusion significantly reduced the degree of renal tissue injury and led to a quick normalization of their structural and functional state. In addition, the administration of the PSH enzyme increased the survival of experimental animals by a factor of more than 1.5. The use of the recombinant chimeric PSH enzyme can be an effective approach in the prevention and treatment of renal ischemia–reperfusion injury, as well as for maintaining an isolated kidney during transplantation.

中文翻译：

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嵌合 PSH 抗氧化酶对肾缺血再灌注损伤的保护作用

摘要——再灌注阶段自由基和活性氧浓度的快速升高是缺血再灌注损伤最危险的阶段。活性氧和生物大分子自由基氧化的次级产物水平的雪崩式增加导致氧化应激的发展。使用外源性抗氧化剂可以降低受影响组织中活性氧的浓度，抑制或纠正氧化应激的进程；因此，它显着降低了缺血-再灌注损伤的严重程度。急性缺血性肾功能衰竭是与缺血再灌注相关的病理的综合列表中最重要的社会问题之一。已在双侧缺血再灌注肾损伤的动物模型中显示了一种嵌合 PSH 抗氧化酶的肾保护作用，该酶包括人过氧还蛋白 6 和大肠杆菌的含锰超氧化物歧化酶。由于超氧化物歧化酶和过氧化物酶的活性，重组嵌合 PSH 蛋白能够中和尽可能多的活性氧。组织学、生化和分子生物学方法表明，在缺血-再灌注前初步施用嵌合 PSH 蛋白可显着降低肾组织损伤的程度，并导致其结构和功能状态的快速正常化。此外，PSH 酶的给药使实验动物的存活率提高了 1.5 倍以上。