Effects of Pristane on Cytochrome P450 Isozyme Expression in Rat Tissues

International Journal of Environmental Research and Public Health

Carolyn B. Howard²  Jacqueline Samuel²  Shalonda B. Henderson²  Jacqueline Stevens²  Paul E. Thomas¹ 

[1]Laboratory for Cancer Research, College of Pharmacy, Rutgers University, Piscataway, NJ 08855-0789, U S A.

[2]Breast Cancer Research Laboratory, Department of Biology, and NIH-Center for Environmental Health, College of Science, Engineering and Technology, Jackson State University, 1400 Lynch Street, P. O. Box 18540, Jackson, Mississippi, USA.

关键词: Pristane;    Cytochrome P450 (CYP);    monoclonal antibodies;    3-methylcholanthrene;    phenobarbital;    Western blots;   

DOI  :  10.3390/ijerph2005010138

来源: mdpi

【 摘 要 】

Chemical carcinogenesis studies are powerful tools to obtain information on potential mechanisms of chemical factors for malignancies. In this study Western blot analyses, using monoclonal antibodies specific for three different cytochrome P450 (CYP) isozymes (CYP1A1, CYP1A2 and CYP2B), were employed to examine the effect(s) of 3-methylcholanthrene and/or pristane (2,6,10,14-tetramethylpentadecane) on the basal and inducible levels of expression of CYP proteins within Copenhagen rat tissues. Pristane exposure led to tissue specific differences in the CYP isozymes expressed and elicited increased CYP protein expression over 3-methylcholanthrene induced levels in microsomes isolated from liver, Peyer’s Patches, and thymus. Within the context of the chemical carcinogenesis model employed in this study, these observations correlated with the induction of B-cell malignancies by low doses of 3-methylcholanthrene and of thymic lymphomas by a high 3-methylcholanthrene dose. The data suggest that pristane treatment affects CYP isozyme expression. This pristane-mediated effect clearly could be a contributing factor in the chemical carcinogenesis of the previously observed lymphoid malignancies, and a possible basis for the tumor enhancing effects of pristane.

【 授权许可】

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