Key result
Doxorubicin and menadione decreased cell proliferation in Saccharomyces cerevisiae by different mechanisms, with menadione inducing G1-phase arrest and doxorubicin inducing G1- and S-phase arrest.
Doxorubicin and menadione decrease cell proliferation in Saccharomyces cerevisiae through distinct mechanisms involving cell cycle arrest and redox pathway modulation.
Hypothesis-generating in yeast; leaves open translation to doxorubicin cardiotoxicity mechanisms in mammals.
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.
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Saenko et al. (2010) studied this question. Doxorubicin and menadione was evaluated on Cell proliferation, cell cycle distribution, glutathione concentration, ribonucleotide reductase expression, and Yap1 pathway activity. Doxorubicin and menadione decreased cell proliferation in Saccharomyces cerevisiae by different mechanisms, with menadione inducing G1-phase arrest and doxorubicin inducing G1- and S-phase arrest.
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