Peroxiredoxin genes are not induced in myeloid leukemia cells exposed to ionizing radiation

Roberta Di Pietro*, H. Fang, K. Fields, S. Miller, M. Flora, E. C. Petricoin, G. Dveksler, R. A. Rana, P. M. Grimley

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

20 Scopus citations


Peroxiredoxins (Prx) comprise an extended family of small antioxidant proteins which conserve a thioredoxin-dependent catalytic function that can contribute to cell protection from reactive oxygen species (ROS). ROS generation is one of the deleterious intracellular effects of ionizing radiation, but the role of Prx during radiation treatment has not been extensively explored. Present experiments measure effects of ionizing radiation on expression of human Prx types I (PAGA), II (NKEF-B) and IV (AOE372) in human myeloid leukemia cells (K562). Prx gene transcription was analyzed by amplifying with RT-PCR cDNAs complementary to each Prx-specific coding sequence and by identifying the derived products with Southern blotting procedure. Transcripts of GAPDH were used as the endogenous standard for semi-quantitative comparisons. No consistent increase in Prx gene expression was detected at time intervals up to 72 h after gamma radiation doses that caused cell cycle arrest and nuclear damage (maximum 20 Gy). Immunoblots also were consistent with a prolonged expression or stability of the Prx I/II proteins. Similarly, a cytotoxic concentration of the oxidant hemin, which stimulates rapid hemoglobinization of K562 cells, caused no induction of Prx gene expression. Our results indicate a high Prx stability in human radio-resistant leukemia cells.

Original languageEnglish
Pages (from-to)517-524
Number of pages8
JournalInternational Journal of Immunopathology and Pharmacology
Issue number3
StatePublished - 2006
Externally publishedYes


  • Ionizing radiation
  • Myeloid leukemia
  • Oxidative stress
  • Peroxiredoxins


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