Effects of polychlorinated biphenyls on porphyrin synthesis and cytochrome p—450—dependent monooxygenases in small intestine and liver of Japanese quail

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Abstract
The effects of acute exposure to polychlorinated biphenyls (PCBs) on porphyrin synthesis and cytochrome P‐450‐dependent monooxygenases in the small intestine and liver were studied in male Japanese quail. The birds were dosed orally with the PCB mixture, Aroclor 1242, or the individual PCB isomers, 2,4,2’,4'‐tetrachlorobiphenyl (2‐TCB) and 3,4,3’,4'‐tetrachlorobiphenyl (3‐TCB), and were killed 48 h later. All the PCB compounds caused a significant increase in porphyrin content and δ‐aminolevulinic acid synthetase (ALA‐S) activity in the small intestine and liver. Increases in porphyrins were greater in the small intestine than in liver. However, a smaller increase in ALA‐S activity occurred in the small intestine than in liver, suggesting that ALA‐S induction is not a major mechanism for the increased porphyrin content of small intestine. All the test compounds significantly increased the cytochrome P‐450 content of liver. In the small intestine, cytochrome P‐450 content was increased by Aroclor 1242 and 2‐TCB but not by 3‐TCB. The activity of 7‐ethoxyresorufin O‐deethylase, however, was increased by all test compounds in both liver and small intestine. In contrast, there was a striking difference between small intestine and liver in the induction of 7‐ethoxycoumarin O‐deethylase (ECOD) activity by Aroclor 1242. In the liver, ECOD activity was unchanged or decreased, but in the small intestine, ECOD activity increased linearly with dose. No tissue difference in ECOD activity was observed after treatment with 2‐TCB or 3‐TCB. These findings suggest that acute exposure to a given PCB results in marked differences between small intestine and liver in porphyrin metabolism and in the induction of cytochrome P‐450 isozymes and associated monooxygenases.

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