Abstract
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 . In this study, an over-expression plasmid carrying PrxI was transfected into mouse embryonic fibroblasts (MEFs) to investigate potential compensatory relationships between PrxI and PrxII. ROS levels induced by oxidative stress were increased in MEFs as compared to wild-type MEFs. Moreover, exposure of MEFs to caused a reduction in cell viability of about 10%, and the proportion of cell death was increased compared to mock-treated MEFs. However, transient over-expression of PrxI in MEFs conferred increased resistance against the oxidative damage, as evidenced by increased cell viability and reduced intracellular ROS levels under stress conditions. The findings suggest that over-expressed PrxI can partly compensate for the loss of PrxII function in PrxII-deficient MEFs.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
