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Biological Sciences , UDC: 616.36:661.833-577 DOI: 10.25688/2076-9091.2023.52.4.04


  • Tymoshenko Yana Evgenievna
  • Yesaulenko Elena Evgenievna Doctor of Biological Sciences
  • Shevchenko Alexey Stanislavovich


Currently, there are no available pharmacological methods of metabolic correction that can provide reliable organ protection during ischemia-reperfusion damage. One of the possible ways of metabolic correction of such damage is the regulation of the activity of oxidative decarboxylation of pyruvate. The purpose of the study is to determine the nature of the effect of sodium dichloroacetate on the development of ischemia-reperfusion damage of the liver under conditions of vascular isolation of the parenchyma in rats. The study was performed on seven groups of rats: a control group, comparison groups (with different models of liver ischemia-reperfusion) and experimental groups, which were administered sodium dichloroacetate 300 mg/kg intraperitoneally before ischemia. As a result of the studies, experimental data were obtained for the first time confirming the decrease in pyruvate dehydrogenase activity after liver ischemia-reperfusion by 70–72 %. This may be one of the key links in the pathogenesis of the developing pathological process, blocking the use of glucose in energy exchange after the blood flow restoration. The use of sodium dichloroacetate was accompanied by an increase in pyruvate dehydrogenase activity by 4,7–5,0 relative to the corresponding comparison groups at the reperfusion stage. Against the background of preliminary administration of sodium dichloroacetate, a decrease in the severity of the cytolytic syndrome was observed according to the determination of the activity of aminotransferases and LDH in the blood plasma, which was 2,0–3,0 times lower than the corresponding indicators in rats in which ischemia-reperfusion was modeled without correction. The data obtained confirm the possibility of reducing the level of hepatocyte cytolysis as well as the level of lactic acidosis and normalizing the prooxidant-antioxidant balance under the condition of preconditioning with sodium dichloroacetate of complete or partial vascular isolation of the rat liver. In this case, the pyruvate dehydrogenase complex can be considered a potential target for mitochondrial cytoprotectors, the impact of which can effectively increase cell resistance to hypoxia.

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Tymoshenko, Y. E., Yesaulenko, E. E. & Shevchenko, A. S. (2023). INFLUENCE OF DICHLOROACETATE ON PYRUVATE DEHYDROGENASE ACTIVITY AND LIVER DAMAGE DURING ISCHEMIA-REPERFUSION IN EXPERIMENTAL CONDITIONS Bulletin of the Moscow City Pedagogical University. Series "Pedagogy and Psychology", 2023, №4 (52), 50. https://doi.org/10.25688/2076-9091.2023.52.4.04
1. 1. Zorova L. D. Functional significance of mitochondrial membrane potential / L. D. Zorova [et al.] // Biological membranes: Journal of Membrane and Cell Biology 2017. Vol. 34. № 6. P. 93–100. (In Russ.). DOI: 10.7868/S0233475517060020
2. 2. Manuilov A. M. Biological activity of sodium dichloroacetate: concepts and mechanisms (literature review) / A. M. Manuilov [et al.]. Kuban Scientific Medical Bulletin. 2016. Vol. 6. № 161. P. 156–163. (In Russ.). DOI: 10.25207/1608-6228-2016-6- 156-163
3. 3. Neymark M. I. Ischemia-reperfusion syndrome. Surgery // Magazine named after N. I. Pirogov. 2021. Vol. 9. P. 71–76. (In Russ.). DOI: 10.17116/hirurgia202109171
4. 4. Popov K. A. Choosing the optimal marker of acute liver injury in rats in an experiment / K. A. Popov [et al.] // Bulletin of the Peoples’ Friendship University of Russia, 2020. Vol. 24. № 4. P. 293–303. (In Russ.). DOI: 10.22363/2313-0245-2020-24-4-293-303
5. 5. Popov K. A. The role of pyruvate dehydrogenase complex in the development of ischemic reperfusion syndrome / K. A. Popov [et al.] // Kuban Scientific Medical Bulletin. 2022. Vol. 29. № 4. P. 75–93. (In Russ.). DOI: 10.25207/1608-6228-2022-29-4-75-93
6. 6. Tsymbalyuk I. Yu. Metabolic correction with sodium dichloroacetate of ischemic reperfusion injury during vascular isolation of the liver in an experiment / I. Yu. Tsymbalyuk [et al.] // News of surgery. 2017. Vol. 25. № 5. P. 447–453. (In Russ.). DOI: 10.18499/2070-478X-2017-10-2-130-136
7. 7. Abudhaise H., Taanman J. W., Fuller B. J. Mitochondrial respiratory chain and Krebs cycle enzyme function in human donor livers subjected to end-ischaemic hypothermic machine perfusion // PLoS ONE. 2021. Vol. 16 (10). P. 257783. DOI: 10.1371/journal.pone.0257783
8. 8. Choi E. K., Jung H., Jeon S. Role of Remote Ischemic Preconditioning in Hepatic Ischemic Reperfusion Injury // Dose-Response. 2020. P. 1–6. DOI: 10.1177/ 1559325820946923
9. 9. Eltzschig H. K., Eckle T. Ischemia and reperfusion-from mechanism to translation // Nat Med. 2011. Vol. 17 (11). P. 1391–1401. DOI: 10.1038/nm.2507
10. 10. Kinnaird A., Dromparis P., Saleme B. Metabolic modulation of clear-cell renal cell carcinoma with dichloroacetate, an inhibitor of pyruvate dehydrogenase kinase // European Urology. 2016. Vol. 69. № 4. P. 734–744. DOI: 10.1016/j.eururo.2015.09.014
11. 11. Schoder H., Knight R. J., Kofoed K. F. Regulation of pyruvate dehydrogenase activity and glucose metabolism in post-ischaemic myocardium // Biochim Biophys Acta. 1998. Vol. 1406 (1). P. 62–72. DOI: 10.1016/s0925-4439(97)00088-4
12. 12. Thibodeau A., Geng X., Previch L. E. Pyruvate dehydrogenase complex in cerebral ischemia-reperfusion injury // Brain Circ. 2016. Vol. 2 (2). P. 61–66. DOI: 10.4103/2394-8108.186256
13. 13. Wu M. Y., Yiang G. T., Liao W. T. Current Mechanistic Concepts in Ischemia and Reperfusion Injury // Cell Physiol Biochem. 2018. Vol. 46 (4). P. 1650–1667. DOI: 10.1159/000489241
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