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[Cancer Research 54, 5797-5800, November 15, 1994]
© 1994 American Association for Cancer Research

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{alpha}-Particle-induced p53 Protein Expression in a Rat Lung Epithelial Cell Strain1

Albert W. Hickman, Richard J. Jaramillo, John F. Lechner and Neil F. Johnson2

Inhalation Toxicology Research Institute, Albuquerque, New Mexico 87185

Other investigators have shown that both sparsely ionizing and UV radiation cause cell cycle arrest that is associated with increased expression of wild-type p53 protein. The effect of exposure to {alpha}-particles from 238Pu on the induction of the p53 protein has now been examined in cultured lung epithelial cells derived from male F344 rats. The number of cells having increased levels of p53 protein was determined by flow cytometry after the cells had been stained with a monoclonal antibody to p53. {alpha}-Particle irradiation caused a dose-dependent increase in p53 protein levels detectable at doses as low as 0.6 cGy, with no evidence of a threshold. An increase in p53 protein also occurred in X-irradiated cells. However, no increase was seen in cells exposed to less than 10 cGy of X-rays, indicating the existence of a relatively higher DNA damage threshold for sparsely ionizing radiation. In addition, more cells exposed to low doses of {alpha} radiation had increased p53 protein levels than would be predicted based on the number of nuclei expected to be traversed by an {alpha}-particle, suggesting that {alpha}-particles cause genetic damage by mechanisms in addition to direct interactions with DNA.

1 This work was supported by the Office of Health and Environmental Research, U.S. Department of Energy, under Contract No. DE-AC04-76EV01013.

2 To whom requests for reprints should be addressed, at Inhalation Toxicology Research Institute, P.O. Box 5890, Albuquerque, NM 87185.

Received 7/ 8/94. Accepted 10/ 3/94.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
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Copyright © 1994 by the American Association for Cancer Research.