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PubMed1995

p53 alterations in plutonium-induced F344 rat lung tumors.

The tumor suppressor gene p53 plays a critical role in the cellular response to genetic damage caused by radiation. In addition, mutations in this gene are often encountered in cells in lung tumors resected from uranium miners whose exposure to radon daughters exceeded 450 working level months. However, most of these miners also smoked tobacco products. Thus whether this gene is of specific importance in lung cancer is unclear. In this study, aberrations in the p53 gene were investigated using an immunohistochemical assay on 38 lung tumors (26 squamous cell carcinomas, 9 adenocarcinomas and 3 adenosquamous carcinomas) from rats that had inhaled 239PuO2 aerosols. Only 2 tumors exhibited detectable levels of staining of p53 products; both were large, well-differentiated squamous cell carcinomas that had invaded the pleural cavity or mediastinum. Direct DNA sequence analysis was used to characterize the mutations in these two tumors, and both exhibited G-->A transition mutations. One tumor was mutated in the first position of codon 283, resulting in a lysine for glutamine substitution; the other tumor was mutated at the second position of codon 280, resulting in a histidine to arginine substitution. No alterations in exons 5-7 of the p53 gene were found in a representative sample of tumors that did not exhibit elevated levels of the protein by immunohistochemistry. Further, no detectable polymorphisms or deletions were observed within the rat p53 gene after Southern blot analysis of 18 randomly selected 239Pu-induced tumors. These results suggest that p53 mutations are relatively unimportant in the development of lung tumors induced in the rat by high-linear energy transfer radiation.

Adenocarcinoma↗
PubMed1994

Plutonium problems.

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Air Pollutants, Radioactive↗
PubMed1993

Duration and dose-related effects of an orally administered, partially lipophilic polyaminocarboxylic acid on the decorporation of plutonium and americium.

A recently developed, orally administered, partially lipophilic polyaminocarboxylic acid-based chelator, docosyl-triethylenetetraminepentaacetic acid (C22TT), was tested for its ability to promote decorporation of 239Pu and 241Am. The effects of dose and duration of treatment were determined in rats injected with 239Pu or 239Pu/241Am 2 weeks before the initiation of C22TT treatment and compared with untreated controls. In the dose-effects study, significant reductions in total body Am content were seen within 3 days after the initiation of C22TT treatment. After 30 days of treatment, there were dose-related reductions in the Pu and Am content of soft tissues and bones. All doses of C22TT resulted in substantial reductions in Pu and Am content of the liver. In the time-response study, there were rapid reductions in total body Am content in the C22TT-treated animals. The greatest reductions occurred within the first 30 days of treatment. Significant decreases in Pu content of soft and hard tissue were observed in the treated animals at 30, 60 or 90 days compared with untreated controls. The greatest reductions in organ Pu content occurred within the first 30 days of treatment, particularly in the liver, but it continued throughout the experiment. Neutron-induced autoradiography showed that C22TT greatly reduced the incorporation of Pu into new bone and substantially reduced the Pu content of the bone marrow. There was no evidence of overt toxicity in either experiment. This study demonstrates that orally administered C22TT is effective in reducing soft and hard tissue content of internally deposited Pu and Am.

Acetates↗