Mitochondrial dysfunction as a mechanism of antitumor and antimetastatic action of hybrid organotin compounds

The article is devoted to the study of the effect of hybrid organotin compounds (OOS) containing a fragment of 2,6-di-tert-butylphenol on the level of mi-tochondrial dysfunction in the mitochondria of the liver and the primary tumor node of tumor ‒ bearing animals (melanoma B16). The aim of the study was to evaluate some markers of oxidative damage and apoptotic processes in mitochondria with a five – fold intraperitoneal administration of bis(3,5-di-tert-butyl-4-hydroxyphenylthiolate) dimethyltin (Me3) and (3,5-di-tert-butyl-4-hydroxyphenylthiolate) triphenyltin (Me5) to C57B1/6 mice 48 hours after transplantation of tumor material (subcutaneously) on models of transplanted melanoma B16 tumors at the maximum effective doses of 375 mg/kg and 250 mg/kg, respectively. Based on the results of the study, it can be concluded that the candidates studied by us for drugs of the antitumor group bis(3,5-di-tert-butyl-4-hydroxyphenylthiolate) dimethyltin (Me3) and (3,5-di-tert-butyl-4-hydroxyphenylthiolate) triphenyltin (Me5) have properties to modulate oxidative stress and apoptotic processes in the mitochondria of tumor – bearing animals with melanoma B16. The obtained data fully correlate with the change in the growth of the primary focus and the activity of metastasis of the tumor process. One of the main targets of the effects of hybrid organotin compounds Me3 and Me5 is the mitochondria.