Yacton and mexicor influence on prooxidant-antioxidant homeostasis and protein synthesis in the myocardium of rats in conditions of doxorubicin cardiomyopathy

Abstract

Doxorubicin, which is included in the scheme of cancer treatment, possesses cardiotoxicity that requires effective cardioprotectors searching. Aim. The aim of the study was to compare the infl uence of yacton and mexicor on the antioxidant system, oxidative modifi cation of proteins, protein synthesis in the myocardium of rats in conditions of doxorubicin cardiomyopathy. Methods and results. The content of prooxidant-antioxidant homeostasis indicators-SOD, GPR, GR, AFG, KFG and proteinsynthesis-the protein content in the cytoplasma and mitochondria and protective effect of derivatives of succinic acid (yacton, mexicor) were studied in the myocardium of rats in the conditions doxorubicin cardiomyopathy with wellknown methods. Conclusion. It is stated that yakton similar to mexicor has protective infl uence on the prooxidant-antioxidant homeostasis, protein synthesis in the rats myocardium in conditions of doxorubicin cardiomyopathy.

Pro-/antioxidant reactions and nitrogen oxide metabolism under sub-chronic effect of succinic acid derivatives

“…belong to drugs of the metabolic action type that enhance energy metabolism and are capable of correcting the free-radical processes [1,2]. Among DSA's, researchers have identified compounds with the antioxidant, detoxifying, anti-hypoxic, anti-diabetic, anti-inflammatory, cardio-and hepatoprotective activity [3][4][5][6].…”

“…belong to drugs of the metabolic action type that enhance energy metabolism and are capable of correcting the free-radical processes [1,2]. Among DSA's, researchers have identified compounds with the antioxidant, detoxifying, anti-hypoxic, anti-diabetic, anti-inflammatory, cardio-and hepatoprotective activity [3][4][5][6].It is known that DSA's serve as exogenous donors of an energy substrate, succinate, oxidation of which within the TCA cycle restores FADH 2 in structure of the succinate dehydrogenase; however, the actual electron acceptance (accompanied by the ATP synthesis) is accomplished by coenzyme Q in the mitochondrial respiratory chain. The stated compounds are able, at hypoxia conditions, to increase the activity of the succinate-oxidase way of oxidation as the compensatory metabolic flux that normali zes the intracellular pool of ATP and thus facilitates the aerobic energy supply [7].…”