Induction of rat liver microsomal and nuclear cytochrome p-450 by dietary 2-acetylaminofluorene and butylated hydroxytoluene
Biochemical Pharmacology, ISSN: 0006-2952, Vol: 38, Issue: 18, Page: 3075-3081
1989
- 14Citations
- 2Captures
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Article Description
The influence of dietary 2-acetylaminofluorene (AAF) on the cytochrome P-450 content of rat liver microsomal and nuclear fractions was immunochemically probed with monoclonal and polyclonal antibodies to cytochromes P-450c and P-450d. Cytochrome P-450d but not P-450c was immunodetected in microsomes, nuclear envelopes, and nuclei from untreated rats. The levels of both cytochromes P-450c and P-450d were elevated after a diet of either 0.1% AAF for 1 week or 0.05% AAF for 3 weeks. However, the level of cytochrome P-450c relative to P-450d was lower after the more prolonged AAF feeding. Supplementation of AAF-containing diets with 0.3% butylated hydroxytoluene (BHT), which affords protection against AAF hepatocarcinogenesis in high-fat fed rats, protected and/or induced total (spectral) nuclear envelope cytochrome P-450 content. Immunochemical studies of liver fractions showed that BHT enhanced the AAF-dependent induction of cytochrome P-450c, but not of P-450d. This was a concerted effect of AAF + BHT since dietary BHT by itself did not affect the levels of cytochrome P-450c or P-450d as compared to control rats. Since 1- to 3-week dietary AAF had little effect on total (spectral analyses) microsomal cytochrome P-450 but markedly reduced total P-450 in nuclear envelopes, the coordinated induction of specific cytochrome P-450s in the different fractions suggests selective induction and depression of different forms of cytochrome P-450 and provides additional evidence for independent regulation of the drug-metabolizing system in nuclear envelope and microsomes. In addition, these results suggest that regulation of cytochrome P-450 may play a crucial role in the nutritional modulation of AAF hepatocarcinogenesis.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/000629528990018X; http://dx.doi.org/10.1016/0006-2952(89)90018-x; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0024444855&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/2783162; https://linkinghub.elsevier.com/retrieve/pii/000629528990018X; http://linkinghub.elsevier.com/retrieve/pii/000629528990018X; http://api.elsevier.com/content/article/PII:000629528990018X?httpAccept=text/xml; http://api.elsevier.com/content/article/PII:000629528990018X?httpAccept=text/plain
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