Characterization of the Dose–Response of CYP1B1, CYP1A1, and CYP1A2 in the Liver of Female Sprague–Dawley Rats Following Chronic Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin

Walker, Nigel J.; Portier, Christopher J.; Lax, Sigurd; Crofts, Frances; Liu, Ying; Lucier, George W.; Sutter, Thomas R.

doi:10.1006/taap.1998.8595

Cited by 87 publications

(46 citation statements)

References 28 publications

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“…These plots also display the reliability of each platform by producing results with the expected trends. Previous literature indicates up-regulation of Cyp1b1 (Walker et al 1999;Boutros et al 2008Boutros et al , 2011 and downregulation of Inmt by TCDD in rodent liver. Our qPCR data for Cyp1b1 show downregulation at low doses (<0.1 mg/kg at 19 h) of TCDD and up-regulation at higher doses in both the TCDDsensitive and TCDD-resistant strains, with OpenArray showing a similar response in just the TCDD-sensitive strain.…”

Section: Discussionmentioning

confidence: 86%

Systematic evaluation of medium-throughput mRNA abundance platforms

Prokopec

Watson

Waggott

et al. 2012

RNA

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Profiling of mRNA abundances with high-throughput platforms such as microarrays and RNA-seq has become an important tool in both basic and biomedical research. However, these platforms remain prone to systematic errors and have challenges in clinical and industrial applications. As a result, it is standard practice to validate a subset of key results using alternate technologies. Similarly, clinical and industrial applications typically involve transitions from a high-throughput discovery platform to medium-throughput validation ones. These medium-throughput validation platforms have high technical reproducibility and reduced sample input needs, and low sensitivity to sample quality (e.g., for processing FFPE specimens). Unfortunately, while medium-throughput platforms have proliferated, there are no comprehensive comparisons of them. Here we fill that gap by comparing two key medium-throughput platforms-NanoString's nCounter Analysis System and ABI's OpenArray System-to gold-standard quantitative real-time RT-PCR. We quantified 38 genes and positive and negative controls in 165 samples. Signal:noise ratios, correlations, dynamic range, and detection accuracy were compared across platforms. All three measurement technologies showed good concordance, but with divergent price/time/sensitivity trade-offs. This study provides the first detailed comparison of medium-throughput RNA quantification platforms and provides a template and a standard data set for the evaluation of additional technologies.

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Section: Discussionmentioning

confidence: 86%

Systematic evaluation of medium-throughput mRNA abundance platforms

Prokopec

Watson

Waggott

et al. 2012

RNA

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“…17,18) The induction mechanism mediated by the Ah-receptor is considered to take place as follows. 19) The Ah-receptor is usually combined with a homodimer of heat shock protein (HSP) 90 that is displaced on ligand binding.…”

Section: Discussionmentioning

confidence: 99%

The Induction of Hepatic Selenium-Binding Protein by Aryl Hydrocarbon (Ah)-Receptor Ligands in Rats.

Ishida

Ishii

Yamada

et al. 2002

JOURNAL OF HEALTH SCIENCE

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Selenium-binding protein (SeBP) is one of the cytosolic proteins which is believed to bind to selenium without containing selenocysteine. Although its physiological role remains to be identified, it has recently attracted interest due to its participation in the late stages of intra-Golgi protein transport. In a previous study, we found that SeBP in rat liver is significantly increased following administration of aryl hydrocarbon (Ah)-receptor ligands, 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) and 3-methylcholanthrene (MC). Little research has been carried out to examine the properties of the inducibility of SeBP by xenobiotics. The objectives of this study were to analyze the control of transcription of the message by Ah-receptor ligands. In this report, we cloned an inducible rat SeBP. The resulting PCR product consisted of the full coding sequence for the 472 amino acids. The deduced amino acid sequence exhibited homologies with mouse SeBP, mouse acetaminophen-binding protein and human SeBP of 92%, 93% and 87%, respectively. We also measured the mRNA level by quantitative reverse transcriptional (RT)-PCR. Treatment of rats with PCB126 resulted in significant induction of the mRNA of this protein in the liver compared with the control level. Our data represent the first report showing that SeBP is induced by an Ah-receptor ligand at the mRNA level.

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“…Metabolism of E 2 to 2-hydroxyestradiol is predominantly catalyzed by cytochrome P450 CYP1A1 (Roy et al, 1992;Spink et al, 1998) with some contribution by members of the CYP3A family (Hammond et al, 1997), while metabolism of E 2 to the 4-hydroxyestradiol is mainly a result of CYP1B1 activity (Spink et al, 1994;Hayes et al, 1996;Jefcoate et al, 2000). In liver, TCDD increases the levels of CYP1A1 and CYP1A2 relative to CYP1B1 (Walker et al, 1999), hence 2-hydroxylation predominates over 4-hydroxylation. Similar results have been reported in several breast epithelial tumor and nontumor cell lines where TCDD strongly induced CYP1A1 activity with resultant 2-hydroxyestradiol formation as the major E 2 metabolite (Spink et al, 1998).…”

Section: Effects Of Gender and Sex Hormones In The Tcdd Dose-responsementioning

confidence: 99%

Induction of Oxidative Stress Responses by Dioxin and other Ligands of the Aryl Hydrocarbon Receptor

et al. 2005

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ᮀTCDD and other polyhalogenated aromatic hydrocarbon ligands of the aryl hydrocarbon receptor (AHR) have been classically considered as non-genotoxic compounds because they fail to be directly mutagenic in either bacteria or most in vitro assay systems. They do so in spite of having repeatedly been linked to oxidative stress and to mutagenic and carcinogenic outcomes. Oxidative stress, on the other hand, has been used as a marker for the toxicity of dioxin and its congeners. We have focused this review on the connection between oxidative stress induction and the toxic effects of fetal and adult dioxin exposure, with emphasis on the large species difference in sensitivity to this agent. We examine the roles that the dioxin-inducible cytochromes P450s play in the cellular and toxicological consequences of dioxin exposure with emphasis on oxidative stress involvement. Many components of the health consequences resulting from dioxin exposure may be attributable to epigenetic mechanisms arising from prolonged reactive oxygen generation.

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Characterization of the Dose–Response of CYP1B1, CYP1A1, and CYP1A2 in the Liver of Female Sprague–Dawley Rats Following Chronic Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin

Cited by 87 publications

References 28 publications

Systematic evaluation of medium-throughput mRNA abundance platforms

Systematic evaluation of medium-throughput mRNA abundance platforms

The Induction of Hepatic Selenium-Binding Protein by Aryl Hydrocarbon (Ah)-Receptor Ligands in Rats.

Induction of Oxidative Stress Responses by Dioxin and other Ligands of the Aryl Hydrocarbon Receptor

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