No abstract

One-month therapy with trimetazidine sharply decreased the content of free radical oxidation products, lipid peroxides and malonic dialdehyde, in atherogenic low-density lipoproteins in patients with coronary heart disease. Activity of glutathione peroxidase utilizing lipid peroxides in the plasma markedly increased during trimetazidine therapy. The data suggest that trimetazidine not directly interacting with free radicals attenuates the adverse effects of intensive free radical oxidation in coronary heart disease. This effect is mediated via activation of antioxidant enzymes, which diminishes negative consequences of ischemia.

Trimetazidine is 2-fold inferior to probucol in antioxidant activity measured using the model of copper-induced free radical oxidation of human plasma lipoproteins. EPR-spectroscopy shows that trimetazidine forms no free-radical intermediates in the presence of generated lipid alkoxyl or hydroxyl radicals, while probucol under these conditions forms phenoxyl radicals. Trimetazidine does not interact with superoxide radicals generated in the xanthinexanthine oxidase system, since it does not inhibit reduction of tetrazolium nitroblue. However, indirect effect of trimetazidine on free radical oxidation cannot be excluded in vivo.