ArticleDrug metabolism and disposition: the biological fate of chemicals2013
Tissue distribution, ontogeny, and chemical induction of aldo-keto reductases in mice.
Article in Drug metabolism and disposition: the biological fate of chemicals, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
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- Epigenetic analysis in a murine genetic model of Gulf War illness.Frontiers in toxicology · 2023Article
- Peripheralized sepiapterin reductase inhibition as a safe analgesic therapy.Frontiers in pharmacology · 2023Review
- Progesterone Metabolism by Human and Rat Hepatic and Intestinal Tissue.Pharmaceutics · 2021Article
- Article
- Pogz deficiency leads to transcription dysregulation and impaired cerebellar activity underlying autism-like behavior in mice.Nature communications · 2020Article
- The influence of biological sex and sex hormones on bile acid synthesis and cholesterol homeostasis.Biology of sex differences · 2019Review
- Regulation of Hepatic Long Noncoding RNAs by Pregnane X Receptor and Constitutive Androstane Receptor Agonists in Mouse Liver.Drug metabolism and disposition: the biological fate of chemicals · 2019Article
- AKR1B1 Upregulation Contributes to Neuroinflammation and Astrocytes Proliferation by Regulating the Energy Metabolism in Rat Spinal Cord Injury.Neurochemical research · 2018Review
- RNA Sequencing Reveals Age and Species Differences of Constitutive Androstane Receptor-Targeted Drug-Processing Genes in the Liver.Drug metabolism and disposition: the biological fate of chemicals · 2017Article
- Merlin controls the repair capacity of Schwann cells after injury by regulating Hippo/YAP activity.The Journal of cell biology · 2017Article
- RNA-Seq reveals common and unique PXR- and CAR-target gene signatures in the mouse liver transcriptome.Biochimica et biophysica acta · 2016Article
- RNA Sequencing Quantification of Xenobiotic-Processing Genes in Various Sections of the Intestine in Comparison to the Liver of Male Mice.Drug metabolism and disposition: the biological fate of chemicals · 2016Article
- Regulation of Hepatic Drug-Metabolizing Enzymes in Germ-Free Mice by Conventionalization and Probiotics.Drug metabolism and disposition: the biological fate of chemicals · 2016Article
- Cytochrome P450 1b1 in polycyclic aromatic hydrocarbon (PAH)-induced skin carcinogenesis: Tumorigenicity of individual PAHs and coal-tar extract, DNA adduction and expression of select genes in the Cyp1b1 knockout mouse.Toxicology and applied pharmacology · 2015Article
- Transcriptome profiling during a natural host-parasite interaction.BMC genomics · 2015Article
- Oxidative and reductive metabolism of lipid-peroxidation derived carbonyls.Chemico-biological interactions · 2015Article
- RNA-sequencing quantification of hepatic ontogeny of phase-I enzymes in mice.Drug metabolism and disposition: the biological fate of chemicals · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Aldo-keto reductases (Akrs) are a conserved group of NADPH-dependent oxido-reductase enzymes. This study provides a comprehensive examination of the tissue distribution of the 16 substrate-metabolizing Akrs in mice, their expression during development, and whether they are altered by chemicals that activate distinct transcriptional factor pathways. Akr1c6, 1c14, 1c20, and 1c22 are primarily present in liver; Akr1a4, 1c18, 1c21, and 7a5 in kidney; Akr1d1 in liver and kidney; Akr1b7 in small intestine; Akr1b3 and Akr1e1 in brain; Akr1b8 in testes; Akr1c14 in ovaries; and Akrs1c12, 1c13, and 1c19 are expressed in numerous tissues. Liver expression of Akr1d1 and Akr1c is lowest during prenatal and postnatal development. However, by 20 days of age, liver Akr1d1 increases 120-fold, and Akr1c mRNAs increase as much as 5-fold (Akr1c19) to 1000-fold (Akr1c6). Treatment of mice with chemical activators of transcription factors constitutive androgen receptor (CAR), pregnane X receptor (PXR), and the nuclear factor-erythroid-2 (Nrf2) transcription factor alters liver mRNAs of Akrs. Specifically, CAR activation by 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) increases mRNAs of Akr1b7, Akr1c6, Akr1c19, and Akr1d1, whereas PXR activation by 5-pregnenolone-16α-carbonitrile (PCN) increases the mRNA of Akr1b7 and suppresses mRNAs of Akr1c13 and Akr1c20. The Nrf2 activator 2-cyano-3,12-dioxooleana-1,9-dien-28-imidazolide (CDDO-Im) induces mRNAs of Akr1c6 and Akr1c19. Moreover, Nrf2-null and Nrf2 overexpressing mice demonstrate that this induction is Nrf2-dependent.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.