Synergistic Effect of Endogenous and Exogenous Aldehydes on Doxorubicin Toxicity in Yeast

Figure 1

Defects in threonine biosynthesis sensitize cells to doxorubicin. Inactivated genes in the threonine biosynthetic pathway result in increased toxicity of doxorubicin (a, b). Inactivation of the HOM3 gene rescues the hom6 strain (c). Quantitation of hom3, hom6, and hom6hom3 survival after doxorubicin exposure, 20 μM (d).

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