Non-growing Escherichia coli cells starved for glucose or phosphate use different mechanisms to survive oxidative stress

Recent data suggest that superoxide dismutases are important in preventing lethal oxidative damage of proteins in Escherichia coli cells incubated und er aerobic, carbon starvation conditions. Here, we show that the alkylhydro peroxide reductase AhpCF (AHP) is specifically required to protect cells in cubated under aerobic, phosphate (Pi) starvation conditions. Additional los s of the HP-I (KatG) hydroperoxidase activity dramatically accelerated the death rate of AHP-deficient cells. Investigation of the composition of spen t culture media indicates that Delta ahpCF katG cells leak nutrients, which suggests that membrane lipids are the principal target of peroxides produc ed in Pi-starved cells. In fact, the introduction of various mutations inac tivating repair activities revealed no obvious role for protein or DNA lesi ons in the viability of ahp cells. Because the death of ahp cells was direc tly related to ongoing aerobic glucose metabolism, we wondered how glycolys is, which requires free Pi, could proceed, P-31 nuclear magnetic resonance spectra showed that Pi-starved cells consumed Pi but were apparently able t o liberate Pi from phosphorylated products, notably through the synthesis o f UDP-glucose. Whereas expression of the ahpCF and katG genes is enhanced i n an OxyR-dependent manner in response to H2O2 challenge, we found that the inactivation of oxyR and both oxyR and rpoS genes had little effect on the viability of Pi-starved cells. In stark contrast, the inactivation of both oxyR and rpoS genes dramatically decreased the viability of glucose-starve d cells.