Gene Expression and DevelopmentsAntioxidant response element-mediated 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induction of human NAD(P)H:Quinone oxidoreductase 1 gene expression
Section snippets
Plasmids
The construction of pNQO1CAT1.55 has been described [3]. Plasmid pNQO1CAT1.55 contains 1.55 kb of the 5′ flanking region and 110 bp of the first exon from the human NQO1 gene. The plasmid pNQO1CAT1.55ΔARE was generated with selected primers and polymerase chain reaction (PCR). The human NQO1 gene promoter was amplified between −1550 and −472 and between −446 and +110 with selected primers and PCR to delete the region between −471 and −447 containing the ARE. The nucleotide sequences of the
Results and discussion
The toxic and mutagenic effects of TCDD are mediated by Ah receptor and XRE-mediated induction of expression of cytochrome P450 genes including the CYP1A1 gene 6, 7. The mechanism of induction of CYP1A1 gene expression by TCDD and Ah receptor is similar to that of members of the super family of steroid receptors 6, 7. It involves binding of TCDD to the Ah receptor, resulting in dissociation of Hsp90 from the Ah receptor and formation of a TCDD-Ah receptor complex. The Ah receptor-TCDD complex
Acknowledgements
This work was supported by NIH Grant GM 47466. We would like to thank Dr. Oliver Hankinson, University of California at Los Angeles, for providing us with the Hepa-1 mutant cell lines.
References (15)
- et al.
Glutathione-S-transferases, structure, regulation, and therapeutic implications
J Biol Chem
(1993) Antioxidant response element
Biochem Pharmacol
(1994)- et al.
Regulation of human NAD(P)H:quinone oxidoreductase gene. Role of AP1 binding site contained within human antioxidant response element
J Biol Chem
(1992) - et al.
Transcriptional regulation of the rat NAD(P)H:quinone reductase gene. Identification of regulatory elements controlling basal level expression and inducible expression by planar aromatic compounds and phenolic antioxidants
J Biol Chem
(1991) - et al.
Human dioxin-inducible cytosolic NAD(P)H:menadione oxidoreductase. cDNA sequence and localization of gene to chromosome 16
J Biol Chem
(1988) - et al.
ARE- and TRE-mediated regulation of gene expressionResponse to xenobiotics and antioxidants
J Biol Chem
(1995) - et al.
A mutation in the aryl hydrocarbon receptor (AHR) in a cultured mammalian cell line identified a novel region of AHR that affects DNA binding
J Biol Chem
(1997)
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2020, Environmental ResearchCitation Excerpt :Then Nrf2 binds to antioxidant/electrophile-response elements (ARE) located in the regulatory regions of many defense enzyme genes to enhance cell survival (Giuliani et al., 2017; Suzuki and Yamamoto, 2015). Initially, Radjendirane and Jaiswal (1999) found that the inducer of AhR could induce the transcriptional expression of the phase II metabolic enzyme (NAD(P)H:quinoneoxidoreductase, NQO1) gene and analyzed the reasons for this phenomenon is the Nrf2-Keap1-AREs pathway could be directly or indirectly activated by TCDD and proposed whether there is an interaction between AhR-ARNT-XREs and Nrf2-Keap1-AREs signaling pathway. Therefore, the current interaction mechanism between AhR-ARNT-XREs and Nrf2-Keap1-AREs signaling pathway is inconclusive, especially whether there is an interaction function between AhR-ARNT-XREs and Nrf2-Keap1-AREs signaling pathway in molluscs and more in-depth studies are still needed in this topic.
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