INFLUENCE OF SYSTEMIC INFLAMMATORY RESPONSE SYNDROME ON THE DEVELOPMENT OF OXIDATIVE STRESS DURING SIMULATION OF CHRONIC ALCOHOL INTOXICATION IN RATS

Biotechnologia Acta Pub Date : 2022-04-01 DOI:10.15407/biotech15.02.062

A. Mykytenko

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Abstract

The aim of our study was to analyze changes in the development of oxidative stress in the liver of rats with chronic alcohol intoxication against the background of systemic inflammatory response syndrome based on the study of catalase and superoxide dismutase activity, concentration of malonic dialdehyde, oxidatively modified proteins and sulfide anion and superoxide anion production. Methods. Experimental studies were performed on 12 male Wistar rats weighing 180‒220 g. Animals were divided into two groups: 1 ‒ control and 2 ‒ animals, on which we simulated alcoholic hepatitis and SIRS. The activity of catalase and superoxide dismutase (SOD), the concentration of malonic dialdehyde (MDA) , oxidatively modified proteins (OMP) sulfide anion and superoxide anion production were studied in the rat liver homogenate. The obtained results were subjected to statistical processing using the Mann-Whitney test. Results. Analyzing the development of oxidative stress in the liver of rats, on which we simulated the combined effects of SIRS and prolonged alcohol intoxication, we found that the activity of SOD increased by 1.72 times (P<0.05), and catalase decreased by 1.18 times (P<0.05) compared with the control group. The production of superoxide anion radical in the liver of rats increased 2.21 times (P<0.05) in the group of animals with combined exposure to bacterial LPS and alcohol intoxication compared to control. The concentration of MDA increased 2.25 times (P<0.05), and OMP by 9.5 times (P<0.05) compared with control group. The concentration of sulfide anion in the liver of rats under the conditions of modeling the combined effects of SIRS and alcohol intoxication decreased by 1.44 times (P <0.05) compared with the control. Conclusions. Modeling of alcohol intoxication against the background of systemic inflammatory response syndrome leads to oxidative damage to lipid and protein structures of the liver due to increased production of superoxide anion radical and imbalance of antiradical protection.

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慢性酒精中毒大鼠模拟过程中全身炎症反应综合征对氧化应激发展的影响

本研究旨在通过对过氧化氢酶和超氧化物歧化酶活性、丙二醛浓度、氧化修饰蛋白以及硫阴离子和超氧化物阴离子产生的研究，分析在全身炎症反应综合征背景下，慢性酒精中毒大鼠肝脏氧化应激发展的变化。方法。对12只体重180-220 g的雄性Wistar大鼠进行了实验研究。将动物分为两组：1组为对照组，2组为动物，在其上模拟酒精性肝炎和SIRS。研究了大鼠肝匀浆中过氧化氢酶和超氧化物歧化酶（SOD）的活性、丙二醛（MDA）的浓度、氧化修饰蛋白（OMP）的硫化物阴离子和超氧化物阴离子的产生。使用Mann-Whitney检验对所获得的结果进行统计处理。后果通过分析大鼠肝脏氧化应激的发展，模拟SIRS和长期酒精中毒的联合作用，发现与对照组相比，SOD活性增加了1.72倍（P<0.05），过氧化氢酶活性降低了1.18倍（P<0.01）。与对照组相比，细菌LPS和酒精中毒联合暴露组大鼠肝脏中超氧阴离子自由基的产生增加了2.21倍（P<0.05）。MDA浓度比对照组增加2.25倍（P＜0.05），OMP增加9.5倍（P＞0.05）。在模拟SIRS和酒精中毒联合作用的条件下，大鼠肝脏中硫阴离子浓度比对照组降低了1.44倍（P<0.05）。结论。在全身炎症反应综合征背景下对酒精中毒进行建模，由于超氧化物阴离子自由基的产生增加和抗自由基保护的失衡，导致肝脏脂质和蛋白质结构的氧化损伤。

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来源期刊

Biotechnologia Acta

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审稿时长

20 weeks