Homologous overexpression of alkyl hydroperoxide reductase subunit C (ahpC) protects Bifidobacterium longum strain NCC2705 from oxidative stress.

The ability to manage reactive oxygen species (ROS) effectively is crucial for the survival of gut bifidobacteria under conditions of oxidative stress. Alkyl hydroperoxide reductase catalytic subunit C (ahpC) of Bifidobacterium longum responds to various oxidative stresses. In this study, an ahpC-overexpressing transformant of B. longum strain NCC2705 was constructed to investigate the role and function of ahpC in oxidative stresses inflicted by treatments with hydrogen peroxide (H2O2), cumene hydroperoxide, and aerobic oxygen. Results indicated that in B. longum, AhpC is the primary scavenger of endogenous H2O2 generated by aerobic metabolism, but it is unable to detoxify high concentrations of exogenous H2O2. The ahpC-overexpressing B. longum strain showed increased resistance to organic hydroperoxide killing, increased viability under aerobic growth, but decreased resistance to exogenous H2O2 in comparison to the control strain. Analysis of genes from the oxidative stress-defense pathway encoding oxygen-independent coproporphyrinogen III oxidase (HemN), NADH oxidase (Nox) and thioredoxin reductase-like protein (TrxB) showed increased transcript levels in the ahpC-overexpressing vs. control strain. These findings suggest that elevated ahpC expression facilitates or activates the different electron donor-dependent ROS-elimination pathways in B. longum's response to oxidative stress.