The role of mitochondria in the development of radiation-induced oxidative stress in K562 leukemia cells.

Radiation-induced accumulation of active oxygen species and the role of the mitochondria in this process were studied on cultured K562 leukemia cells. Intracellular concentrations of active oxygen species in the presence of rotenone and without it and the mitochondrial potential were analyzed 15, 30 min, 1, 4, 8, 12, 24, and 48 h after X-ray exposure in doses of 4 and 12 Gy. Radiation-induced generation of active oxygen species had two time peaks: 30 min and 24 h after the exposure. Addition of rotenone reduced the levels of active oxygen species 24 and 48 h after the exposure. Increase of active oxygen species concentrations was paralleled by an increase of the mitochondrial potential. The mitochondria were responsible for the increase in the concentrations of active oxygen species 12-48 h after irradiation.

[Doxorubicin and menadione reduce cell proliferation of Saccharomyces cerevisiae by different mechanisms].

The aim of this study was to determine the impacts of doxorubicin and menadion on cell proliferation, cell distribution in accordance with the phases of the cell-cycle phase, glutathione concentration, ribonucleotide reductase expression, and Yap1 dependent redox-sensitive pathway activity using Saccharomyces cerevisiae as eukaryote cell model. Our data show that menadione induced cell cycle arrest in G1-phase, reduction of intracellular GSH, an increase in GSSG concentration, and dose-dependent increases in ribonucleotide reductase expression and the activity of Yap1 pathway. Doxorubicin induced cell cycle arrest in G1- and S-phases, increased GSH and GSSG concentrations, increased expression of ribonucleotide reductase, and modulated Yap-dependent pathway activity.

[Combined effect of doxorubicine and dehydroepiandrosterone on proliferation and oxidative stress in Saccharomyces cerevisiae cells].

Results of a comparative study of the influence of doxorubicine (DOX) and dehydroepiandrosterone (DHEA) on cell proliferation and oxidative stress in Saccharomyces cerevisiae cells are presented. Three treatment schedules were assessed--DOX only, DHEA only, and DOX simultaneously with DHEA--in examining cell proliferation, measuring the content of glutathione, and evaluating the expression of ribonucleotide reductase in the test cells. The results indicate that the separate treatment with DOX or DHEA stimulates the expression of ribonucleotide reductase and leads to a decrease in the rate of cell proliferation. DHEA produces a dose-dependent decrease in the content of a reduced form of glutathione in cells, whereas the concentration of the oxidized form remains unchanged. In contrast, the treatment with DOX increased the concentrations of both forms of glutathione. The simultaneous treatment of cells by DOX and DHEA increased the accumulation of intracellular glutathione and decreased the total antiproliferative effect.