AI Article Synopsis
- The aryl hydrocarbon receptor (AHR) is important for regulating responses to environmental pollutants and has physiological roles.
- Adrenalectomized rats show reduced levels of hepatic AHR protein without changes in mRNA, leading to impaired cytochrome P450 1B1 induction, similar to certain mouse models.
- The study found that adrenalectomy and acute dexamethasone treatment did not affect hepatic AHR-interacting protein or other chaperone proteins, indicating that decreased AHR protein levels in rats post-ADX are not linked to changes in these proteins.
Article Abstract
The aryl hydrocarbon receptor (AHR) plays physiological roles and mediates adaptive and toxic responses to environmental pollutants. Adrenalectomized rats display decreased hepatic AHR protein levels, with no change in mRNA, and selectively impaired induction of cytochrome P450 1B1. This is similar to reported phenotypes for mice with hepatocyte-specific conditional deletion of AHR-interacting protein (AIP), a chaperone protein of the cytoplasmic AHR complex. In this study, we demonstrated that adrenalectomy (ADX) and acute dexamethasone (DEX) treatment do not alter hepatic AIP mRNA or protein levels. Also, hepatic protein levels of the 90 kDa heat shock protein and p23 were not altered by ADX or acute DEX treatment. These results suggest that the loss of rat hepatic AHR protein following ADX cannot be explained by changes in the levels of the receptor's cytoplasmic chaperone proteins.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3858301 | PMC |
| http://dx.doi.org/10.1139/cjpp-2013-0238 | DOI Listing |
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