An analysis of the clinical manifestations of complications caused by the toxic effect of chemotherapeutic drugs used in the treatment of malignant neoplasms was carried out. The variety of clinical symptoms that develop against the background of chemotherapy for malignant neoplasms leads to difficulties in differential diagnosis of a primary neurological disease and the identification of complications during treatment. The severity of these complications depends on a number of factors, including the drug used, its dosage and duration of use, the use of various methods of combination therapy and radiation methods, as well as the presence of comorbid pathology in patients. A clear understanding of the mechanisms of development of neurotoxicity and timely diagnosis of such conditions is a priority task of modern clinical medicine Modern methods of treating patients with malignant neoplasms should be based on a multidisciplinary medical approach, including a set of measures to prevent unwanted toxic effects of treatment, stratify individual mortality risks and develop methods of rehabilitation and medical examination.

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Background. One of the key components of energy metabolism is the pyruvate dehydrogenase complex (PDC), the activity of which can be targeted by some cytoprotectors. However, their role remains unclear. It is known that the activation of the PDC in tumor cells leads to an inversion of anaerobic glycolysis with an increase in the generation of free radicals in the respiratory chain and a decrease in viability. At the same time, there is evidence of increased resistance of normal cells to hypoxia and reperfusion.Objectives. Analysis of current information on the role of PDC in the development of pathologic biochemical changes in ischemic reperfusion syndrome and methods of metabolic correction using agents for regulating the activity of the considered multienzyme complex. Methods. The bibliographical search was carried out across the eLIBRARY and PubMed databases with a selection of articles published over the past 10 years in the English and Russian languages, as well as some parts of fundamental works in the selected field, published more than 10 years. To be selected for bibliographical review, the article can be of any design, reflecting the ideas about the role of PDC in the development of pathologic biochemical changes in ischemic-reperfusion lesions of various organs and tissues.Results. The bibliographical analysis indicates a decrease in the activity of PDC in myocardial tissue during a heart attack or heart failure, the activity of the enzyme in skeletal muscles decreases against the background of acute hypoxia. PDC activity also decreases under chronic stress and extensive muscular exercise. At the same time, the PDC activity remains at the normal level in the ischemic period, and the transition to the reperfusion period is accompanied by a sharp decrease in the activity of the multienzyme complex. The PDC inactivation occurring under these conditions can result from a damage by reactive oxygen species, as well as by regulatory control changes through phosphorylation/dephosphorylation. Assuming the key role of PDC in the development of energy exchange disorders against the ischemic-reperfusion injuries 2 main strategies might be offered for metabolic correction: 1) an increase in the activity of PDC (activator — sodium dichloroacetate) or compensation for its lack with substrates of the tricarboxylic acids (acetylcarnitine, β-ydroxybutyrate); 2) protection of PDC from damage (antioxidants).Conclusion. The basis of energy exchange disorders in the reperfusion period is a decrease in PDC activity, and modification of its activity is a promising direction for metabolic prevention or correction of ischemic-reperfusion injures.