Effect of a Prudhoe Bay crude oil on hepatic and renal peroxisomal {beta}-oxidation and mixed-function oxidase activities in rats

• Published in: Carcinogenesis
• Main Authors: Khan, S., Codner, M., Payne, J.F., Rahimtula, A.D.
• Format: Text
• Language: English
• Published: Oxford University Press 1989
• Subjects: ORIGINAL ARTICLES; Prudhoe Bay
• Online Access: http://carcin.oxfordjournals.org/cgi/content/short/10/2/269; https://doi.org/10.1093/carcin/10.2.269

The effect of oral administration of a Prudhoe Bay crude oil (PBCO) to male rats (PBCO, 2.6 g/kg body weight, daily) for 5–12 days on hepatic and renal microsomal mono-oxygenase activities and peroxisomal β-oxidation has been investigated. PBCO administration leads to liver enlargement. This is associated with induction of microsomal cytochrome P-450 levels (1.6- to 2.0-fold) and dependent mixed-function oxidase activities (7-ethoxyresorufin- O -deethylase and 7-pentoxyresorufin- O -depentylase, representing cytochrome P-450I and cytochrome P-450IIB isoenzymes respectively, 9-to 15-fold; ω-oxidation of lauric acid representing the cytochrome P-450IVA1 isoenzyme, 1.4- to 1.5-fold) along with peroxisomal β-oxidation (palmitoyl CoA oxidation, 2- to 5-fold). It was observed that rats exposed to PBCO showed an increase in renal microsomal cytochrome P-450 content (1.6- to 2.3-fold), cytochrome P-450I activity (5- to 8-fold) and ω-oxidation activity (1.3- to 1.4-fold). However, renal peroxisomal β-oxidation was unaltered. Serum total triglycerides were lowered by 41–46% after PBCO exposure. These results suggest that induction of peroxisomal β-oxidation and possibly mono-oxygenases may be related to the carcinogenic/tumorigenic potential of crude oil.