Adaptive response is differently induced depending on the sensitivity to radiation-induced cell death in mouse epidermal cells

S. J. Lee, S. A. Choi, C. K. Cho, T. H. Kim, K. S. Jeong, S. Y. Yoo, Y. S. Lee

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20 Scopus citations


We investigated the relationship between induction of radio-adaptive response and cell death in mouse normal and neoplastic epidermal cells. Mouse normal primary keratinocytes (PK), cancerprone cells [v-ras(Ha)-transfected mouse keratinocytes (ras-PK), and line 308 cells (mouse skin papilloma cells which have activated ras(Ha) gene with A-to-T transversion at codon 61) were primed with a low dose of γ-rays (0.01 Gy), and were challenged with a high dose (4 Gy) after a 4 or 7 h interval. The induction of cell death in PK was 2-10 times higher and was also more rapid in PK than in ras-PK or 308 cells. Low-dose pretreatment with a 4 h interval decreased cell death, and this adaptive response was prominent in PK, whereas it was less obvious in the cases of ras-PK and 308 cells. The response of each protein kinase C (PKC) isozymes to high-dose radiation, especially PKCα, PKCδ, PKCε, and PKCη, were different between the normal and ras oncogene-activated neoplastic keratinocytes; translocation of these isozymes to membrane occurred more rapidly in normal than in neoplastic cells. Furthermore, low-dose pretreatment did not induce the translocation of PKCδ in PK significantly more than in ras-PK and 308. Thus, the difference in the induction of radio-adaptive responses between mouse normal and neoplastic epidermal cells reflects difference in the rapidity of cell death, and responsiveness of PKC may affect this adaptive response.

Original languageEnglish
Pages (from-to)175-184
Number of pages10
JournalCell Biology and Toxicology
Issue number3
StatePublished - 2000

Bibliographical note

Funding Information:
We thank Mr. Kyung-Jung Kim for his excellent technical assistance. This work was supported by a National Nuclear R&D Program from the Ministry of Science and Technology of Korea.


  • Adaptive response
  • Cell death
  • Neoplastic cells
  • Normal cells
  • Protein kinase C


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