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Abstract
Propylene is hepatotoxic to male Charles River COBS Sprague‐Dawley rats pretreated with polychlorinated biphenyls (PCB: Aroclor 1254). Four‐hour inhalation exposure to 50,000 ppm propylene increased liver weight/body weight ratios and elevated serum enzyme activities in PCB‐pretreated animals.
Hepatic microsomal cytochrome P‐450 content of PCB‐pretreated rats dropped profoundly during propylene exposure and remained depressed for at least 24 h. In addition, PCB‐pretreated, propylene‐exposed rats exhibited a decrease in the specific activity of hepatic microsomal aniline hydroxylase. However, there was no change in activities of either hepatic microsomal aminopyrine demethylase or glucose‐6‐phosphatase.
Propylene exposure of rats pretreated with p‐naphthoflavone (BNF), phenobarbital (PB), or a mixture of BNF and PB was not hepatotoxic. However, there was, in these animals, a substantial decline in hepatic microsomal cytochrome P‐450 levels 24 h after the start of propylene exposure. Hence, the propylene‐dependent process resulting in hepatic cytochrome P‐450 destruction is qualitatively or quantitatively different from the process that causes acute hepatotoxicity.
Preexposure fasting had no effect on the hepatotoxicity resulting from a 4‐h exposure of PCB‐pretreated rats to 50,000 ppm propylene. Administration of SKF‐525A to PCB‐pretreated rats immediately prior to propylene exposure completely prevented elevations in serum enzyme activities and liver weight/body weight ratios.
In vitro incubation of hepatic microsomes prepared from either BNF‐, PB‐, or PCB‐pretreated rats with an atmosphere of 20% propylene/80% air produced in NADPH‐dependent decrease in cytochrome P‐450 content.
These results suggest that PCB pretreatment is a prerequisite for propylene hepatotoxicity in the rat. Cytochrome P‐450‐dependent bioactivation of propylene is associated with this hepatotoxicity, but further studies are needed to characterize the mechanism of the PCB‐propylene interaction.
