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). Prxl and Prxl I are more than 90% homologous in their amino acid sequences, and both proteins reduce H(2)O(2). In this study, an over-expression plasmid carrying Prxl was transfected into PrxII(-/-) mouse embryonic fibroblasts (MEFs) to investigate potential compensatory relationships between Prxl 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(2)O(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 Prxl in PrxII(-/-) MEFs conferred increased resistance against the oxidative damage, as evidenced by increased cell viability and reduced intracellular ROS levels under H(2)O(2) stress conditions. The findings suggest that over-expressed Prxl can partly compensate for the loss of Prxl I function in PrxII-deficient MEFs.