Graduate Thesis Or Dissertation
 

Biochemical effects of tumorigenic enhancers

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  • 2 -acetylaminofluorene -induced hepatocarcinogenesis in rats proceeds in stages of initiation and promotion, similar to experimental systems, in mouse skin. In this study promoters of liver tumorigenesis, phenobarbital, DDT and butylated hydroxytoluene (BHT), were compared to non-promoters, amobarbital, diphenylhydantoin (DPH) and benz(a)anthracene (BA), for their ability to cause liver growth when administered acutely. Hepatomegaly and signs of liver hyperplasia paralleled enhancing activity in the cases of phenobarbital, DDT, amobarbital and DPH. Stimulation of liver growth and DNA synthesis by BHT was dose-related, which correlated with its characteristics as a promoter also. However, BA, a non-promoter, stimulated liver growth and DNA synthesis in a manner analogous to phenobarbital and DDT. It is concluded that the mechanism of promotion may involve the stimulation of liver growth, but criteria in addition to increased liver size and DNA synthesis are needed to characterize the nature of the liver growth associated with promotion. Increased nucleocytoplasmic transport of messenger RNA was investigated as a possible mechanism of phenobarbital-induced liver growth. A cell-free assay system was developed in which the release of messenger RNA from isolated rat liver nuclei was dependent upon the concentration of cytosol protein in the incubation medium. Cytosol from phenobarbital-treated liver was found not to differ from control cytosol in stimulating the release of messenger RNA. It is concluded that increased messenger RNA transport is probably not involved in the mechanism of the acute hepatomegaly caused by phenobarbital.
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  • File scanned at 300 ppi (Monochrome) using Capture Perfect 3.0.82 on a Canon DR-9080C in PDF format. CVista PdfCompressor 4.0 was used for pdf compression and textual OCR.
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