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논문 기본 정보

자료유형
학술저널
저자정보
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)
저널정보
한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제19권 제4호
발행연도
2011.1
수록면
451 - 459 (9page)

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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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