Biomolecules & Therapeutics

The Korean Society of Applied Pharmacology (한국응용약물학회)
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Over-expressed Peroxiredoxin I Protects against Oxidative Damage in Mouse Embryonic Fibroblasts Lacking Peroxiredoxin II

  • Kim, Seong-Gon (School of Life Science and Biotechnology, Kyungpook National University) ;
  • Kim, Jae-Young (Department of Biochemistry, School of Dentistry, IHBR, Kyungpook National University) ;
  • Ryoo, Zae-Young (School of Life Science and Biotechnology, Kyungpook National University) ;
  • Lee, Sang-Gyu (School of Life Science and Biotechnology, Kyungpook National University)
  • Received : 2011.07.29
  • Accepted : 2011.10.05
  • Published : 2011.10.30
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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 $H_2O_2$. 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.

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References

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