Peroxiredoxin III-deficiency sensitizes macrophages to oxidative stress

As a mitochondrial scavenger of reactive oxygen species (ROS), peroxiredoxin III (PrxIII) plays an important role in regulating intracellular ROS level. We previously found that PrxIII knockout (PrxIII^-/-) mice were more sensitive than wild-type (PrxIII^+/+) controls to intratracheal inoculation of lipopolysaccharide (LPS), but the precise mechanism remained to be obscure. In the present study, we detected the levels of ROS and tumour necrosis factor alpha (TNF-α) in mouse bone-marrow-derived macrophages. LPS stimulation induced transient increase of ROS production and augmentation of TNF-α accumulation in PrxIII^-/- macrophages. In addition, we observed reduced viability and increased apoptosis in PrxIII ^-/- macrophages exposed to LPS. Our results provide direct evidence that PrxIII is necessary for macrophages to protect against LPS-induced oxidative stress.