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Abstract
1. Investigations in our laboratory have demonstrated a rapid suppression of the P4502b isoform in mouse lung, concomitant with significant induction of this enzyme in liver from these same animals. The current study was designed to determine whether the suppression by polychlorinated biphenyls of pulmonary P4502b required the presence of a functional Ah receptor, and additionally to delineate the time course of the induction responses to Aroclor 1254 in the liver, kidney, and intestine of the AH-responsive and non-responsive mouse.
2. P450s were quantified by specific enzyme assay and immunoblot in liver (1a-1, 1a-2, 2b), lung (1a-1, 1a-2), kidney (1a-1, 1a-2, 2b) and small intestine (1a-1, 2b) of C57 and DBA animals at varying times (48 h-12 weeks) following a single intraperitoneal dose of Aroclor 1254(250mg/kg).
3. The suppression of constitutive P4502b in the lung by Aroclor was observed in both strains, but was more prominent over a longer time course in the non-responsive animals. P4502b enzyme activity was increased in the liver and intestine of both strains of mouse; however, there was a significantly greater response to Aroclor in the C57 animals. These data indicate that the AH receptor does not participate in the suppression of pulmonary P4502b, and suggests that the regulation of inducible P4502b in liver and intestine is quantitatively different between these two strains of mouse.
4. P4501a was predictably induced in all tissues examined from the C57 animal, but was largely unaffected by PCBs in the DBA strain. P4501a-2, which is also regulated by the Ah receptor, was highly induced in the liver of the responsive strain, and also increased approximately two-fold in the liver of the non-responsive animals. Kidney P4501a-2 was also modestly increased by Aroclor, only in the responsive mouse.