Heterogeneity in c-jun gene expression in normal and malignant cells exposed to either ionizing radiation or hydrogen peroxide

Journal Article · Mon May 01 04:00:00 EDT 1995 · Radiation Research

DOI:https://doi.org/10.2307/3579028· OSTI ID:81182

Collart, F R; Horio, M; Huberman, E ^[1]

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1. Argonne National Laboratory, IL (United States)

We investigated the role of reactive oxygen intermediates and protein kinase C in the induction of expression of the c-jun gene in human ML-2 leukemic cells and normal human DET-551 fibroblasts by comparing the effects of exposure to either ionizing radiation or H{sub 2}O{sub 2} in the presence or absence of appropriate inhibitors. In these cell types, the radiation-and H{sub 2}O{sub 2}-mediated increase in c-jun mRNA levels could be prevented by pretreatment of the cells with N-acetylcysteine, and antioxidant, or H7, an inhibitor of protein kinase C and protein kinase A, but not by HA1004, a specific inhibitor of protein kinase A and G. These results suggest a role for protein kinase C and reactive oxygen intermediates in the induction of c-jun gene expression in both normal and tumor cells. We also investigated potential differences in c-jun gene expression induced by radiation or H{sub 2}O{sub 2} in normal and tumor cells by examining steady-state c-jun mRNA levels in a number of human fibroblast, leukemia, melanoma, sarcoma and carcinoma cell types. We observed heterogeneity in the steady-state level of c-jun mRNA in both the untreated normal and tumor cells and in such cells exposed to ionizing radiation or to H{sub 2}O{sub 2}. Exposure to radiation produced a varied response which ranged from little or no induction to an increase in the steady-state level of the c-jun mRNA of more than two orders of magnitude. Exposure to H{sub 2}O{sub 2} gave a pattern similar to that of ionizing radiation. The basis for the differential induction in response to these agents may be attributable to either cell lineage or genetic heterogeneity or a combination of these two parameters. 30 refs., 7 figs., 1 tab.

• Research Organization: Argonne National Laboratory (ANL), Argonne, IL
• DOE Contract Number: W-31109-ENG-38
• OSTI ID: 81182
• Journal Information: Radiation Research, Journal Name: Radiation Research Journal Issue: 2 Vol. 142; ISSN 0033-7587; ISSN RAREAE
• Country of Publication: United States
• Language: English

Related Subjects

56 BIOLOGY AND MEDICINE
APPLIED STUDIES
BIOLOGICAL RADIATION EFFECTS
COMPARATIVE EVALUATIONS
FIBROBLASTS
GENE REGULATION
HYDROGEN PEROXIDE
INDUCTION
IONIZING RADIATIONS
LEUKEMIA
OXYGEN
PHOSPHOTRANSFERASES
RESPONSE MODIFYING FACTORS
TUMOR CELLS