Abstract
Inhalation of diesel exhaust (DE), which contains soot particles with adsorbed mutagenic organic compounds, and its virtually mutagen-free soot particle analog, carbon black (CB), produce similar types and prevalences of pulmonary neoplasms in chronically exposed F344 rats. This result suggests that DE-induced neoplasia develops from the effects of a high lung burden of carbonaceous particles rather than from the genotoxicity of organic constituents. In this investigation, pulmonary carcinomas from rats exposed to DE or CB were analyzed for alterations in K-ras and p53 to determine if mutations caused by these agents are also similar. K-ras and p53 were chosen for this study because mutation patterns of these genes in lung neoplasms have been associated with specific exposures. A low frequency (3/50) and variable pattern of activating mutations were identified in codons 12 and 61 of the K-ras gene. Immunoreactive levels of p53 protein, suggesting gene dysfunction, were present in 7/13 squamous cell or adenosquamous carcinomas, regardless of the associated exposure. However, single-strand conformational polymorphism analysis and direct sequencing of p53 did not detect any mutations in these neoplasms. No immunoreactivity or muta...Continue Reading
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