Over-expressed peroxiredoxin I protects against oxidative damage in mouse embryonic fibroblasts lacking peroxiredoxin II

Peroxiredoxins (Prxs) have a critical role in protecting cells against oxidative damage generated by reactive oxygen species (ROS). PrxI and PrxII are more than 90% homologous in their amino acid sequences, and both proteins reduce H ₂O ₂. In this study, an over-expression plasmid carrying PrxI was transfected into PrxII ^-/- mouse embryonic fibroblasts (MEFs) to investigate potential compensatory relationships between PrxI and PrxII. ROS levels induced by oxidative stress were increased in PrxII ^-/- MEFs as compared to wild-type MEFs. Moreover, exposure of PrxII ^-/- MEFs to H ₂O ₂ caused a reduction in cell viability of about 10%, and the proportion of cell death was increased compared to mock-treated PrxII ^-/- MEFs. However, transient over-expression of PrxI in PrxII ^-/- MEFs conferred increased resistance against the oxidative damage, as evidenced by increased cell viability and reduced intracellular ROS levels under H ₂O ₂ stress conditions. The findings suggest that over-expressed PrxI can partly compensate for the loss of PrxII function in PrxII-deficient MEFs.