scholarly journals Comparisons of Brain, Uterus, and Liver mRNA Expression for Cytochrome P450s, DNA Methyltransferase-1, and Catechol-O-Methyltransferase in Prepubertal Female Sprague-Dawley Rats Exposed to a Mixture of Aryl Hydrocarbon Receptor Agonists

2005 ◽  
Vol 86 (1) ◽  
pp. 175-184 ◽  
Author(s):  
D. Desaulniers ◽  
G.-H. Xiao ◽  
K. Leingartner ◽  
I. Chu ◽  
B. Musicki ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Mrna Expression ◽  
Dna Methyltransferase ◽  
Cytochrome P450s ◽  
Dna Methyltransferase 1 ◽  
Sprague Dawley ◽  
Receptor Agonists ◽  
Aryl Hydrocarbon ◽  
Sprague Dawley Rats ◽  
Methyltransferase 1

scholarly journals A novel 4 S [3H]β-naphthoflavone-binding protein in liver cytosol of female Sprague–Dawley rats treated with aryl hydrocarbon receptor agonists

2000 ◽  
Vol 347 (3) ◽  
pp. 787-795
Author(s):  
Damian BRAUZE ◽  
Danuta MALEJKA-GIGANTI
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Rat Liver ◽  
Binding Protein ◽  
Female Rats ◽  
Sprague Dawley ◽  
Methyltransferase Activity ◽  
Liver Cytosol ◽  
Aryl Hydrocarbon ◽  
Sprague Dawley Rats ◽  
S Peak

β-Naphthoflavone (β-NF) is a widely used inducer of phase-I and phase-II enzymes controlled by aryl hydrocarbon receptor (AhR). Studies of competitive binding with 3H-labelled 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 3-methylcholanthrene (3-MC) and benzo[a]pyrene (B[a]P) have shown that β-NF is a high-affinity ligand for AhR and also for polycyclic aromatic hydrocarbon (PAH)-binding protein, both soluble proteins of rat liver in 8 S and 4 S fractions, respectively, of sucrose gradients. This study examined binding of [3H]β-NF to liver cytosolic proteins of female Sprague-Dawley rats. Treatment of rats with β-NF, 3-MC, TCDD or α-naphthoflavone (α-NF) increased the specific [3H]β-NF binding to liver cytosol up to 125-fold that of vehicle (corn oil)-treated rats (< 100 fmol/mg of protein). Sucrose gradients revealed a large 4 S and a small 8 S peak of radioactivity from [3H]β-NF binding to cytosols of β-NF-, 3-MC-, TCDD- or α-NF-treated rats. Whereas co-incubation with the unlabelled β-NF eliminated both peaks, co-incubation with 2,3,7,8-tetrachlorodibenzofuran (TCDF) eliminated only the 8 S peak. The sucrose density gradient from [3H]TCDD binding to cytosol of β-NF- or TCDD-treated rats yielded a small 4 S and a larger 8 S peak; only the latter was abolished by co-incubation with TCDF. Thus, the patterns of sedimentation, distribution and elimination of radioactivity from the 8 S fraction of the liver cytosols from β-NF-, 3-MC-, TCDD- or α-NF-treated rats were characteristic for the AhR, whereas those from the 4 S fraction appeared specific for [3H]β-NF binding. The data indicate that potent AhR agonists, TCDD, 3-MC and β-NF, and to a lesser extent α-NF, a weak AhR agonist, induce a 4 S [3H]β-NF-binding protein in liver cytosol of female rats. α-NF, β-NF and 3-MC were effective competitors (80-85% inhibition) of the [3H]β-NF-specific binding to the β-NF-, 3 MC- or TCDD-induced 4 S protein, whereas several PAHs including B[a]P and benzo[e]pyrene were only weak competitors. The increased [3H]β-NF binding was not associated with glycine N-methyltransferase activity. Hence, the 4 S [3H]β-NF-binding protein described herein differs from the constitutive 4 S PAH-binding protein of rat liver cytosols in the inducibility by β-NF and 3-MC, ligand-binding characteristics, and lack of glycine N-methyltransferase activity. Gel filtration on Sephacryl of liver cytosols from β-NF-treated rats indicated a molecular mass of ≈ 42 kDa for [3H]β-NF-bound protein and suggested that it was derived from a large mass component that before the radioligand binding was eluted with the void volume of the gel and sedimented in a 7 S fraction of the sucrose gradient. The [3H]β-NF binding activity was not eluted with glutathione S-transferase Ya, aldehyde-3-dehydrogenase or DT-diaphorase [NAD(P)H: quinone oxidoreductase] activities, which are AhR-controlled and β-NF-inducible. Further studies are needed to determine the identity and function of this novel protein which may be involved either directly or indirectly (as a carrier protein) in xenobiotic metabolism in vivo.

scholarly journals Toxicological characterisation of two novel selective aryl hydrocarbon receptor modulators in Sprague-Dawley rats

2017 ◽  
Vol 326 ◽  
pp. 54-65 ◽  
Author(s):  
Selma Mahiout ◽  
Jere Lindén ◽  
Javier Esteban ◽  
Ismael Sánchez-Pérez ◽  
Satu Sankari ◽  
...  
Keyword(s):  
Aryl Hydrocarbon Receptor ◽  
Sprague Dawley ◽  
Aryl Hydrocarbon ◽  
Sprague Dawley Rats ◽  
Receptor Modulators

scholarly journals Effects of a high-fat diet and global aryl hydrocarbon receptor deficiency on energy balance and liver retinoid status in male Sprague-Dawley rats

2021 ◽  
Vol 95 ◽  
pp. 108762
Author(s):  
Raimo Pohjanvirta ◽  
Ira Karppinen ◽  
Suylen Galbán-Velázquez ◽  
Javier Esteban ◽  
Helen Håkansson ◽  
...  
Keyword(s):  
Energy Balance ◽  
Aryl Hydrocarbon Receptor ◽  
High Fat Diet ◽  
Sprague Dawley ◽  
High Fat ◽  
Aryl Hydrocarbon ◽  
Sprague Dawley Rats

scholarly journals Aryl hydrocarbon receptor is essential for the pathogenesis of pulmonary arterial hypertension

2021 ◽  
Vol 118 (11) ◽  
pp. e2023899118
Author(s):  
Takeshi Masaki ◽  
Makoto Okazawa ◽  
Ryotaro Asano ◽  
Tadakatsu Inagaki ◽  
Tomohiko Ishibashi ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Aryl Hydrocarbon Receptor ◽  
Vascular Lesions ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Aryl Hydrocarbon ◽  
Sprague Dawley Rats ◽  
Pulmonary Arterial

Pulmonary arterial hypertension (PAH) is a devastating disease characterized by arteriopathy in the small to medium-sized distal pulmonary arteries, often accompanied by infiltration of inflammatory cells. Aryl hydrocarbon receptor (AHR), a nuclear receptor/transcription factor, detoxifies xenobiotics and regulates the differentiation and function of various immune cells. However, the role of AHR in the pathogenesis of PAH is largely unknown. Here, we explore the role of AHR in the pathogenesis of PAH. AHR agonistic activity in serum was significantly higher in PAH patients than in healthy volunteers and was associated with poor prognosis of PAH. Sprague–Dawley rats treated with the potent endogenous AHR agonist, 6-formylindolo[3,2-b]carbazole, in combination with hypoxia develop severe pulmonary hypertension (PH) with plexiform-like lesions, whereas Sprague–Dawley rats treated with the potent vascular endothelial growth factor receptor 2 inhibitors did not. Ahr-knockout (Ahr−/−) rats generated using the CRISPR/Cas9 system did not develop PH in the SU5416/hypoxia model. A diet containing Qing-Dai, a Chinese herbal drug, in combination with hypoxia led to development of PH in Ahr+/+ rats, but not in Ahr−/− rats. RNA-seq analysis, chromatin immunoprecipitation (ChIP)-seq analysis, immunohistochemical analysis, and bone marrow transplantation experiments show that activation of several inflammatory signaling pathways was up-regulated in endothelial cells and peripheral blood mononuclear cells, which led to infiltration of CD4+ IL-21+ T cells and MRC1+ macrophages into vascular lesions in an AHR-dependent manner. Taken together, AHR plays crucial roles in the development and progression of PAH, and the AHR-signaling pathway represents a promising therapeutic target for PAH.

scholarly journals DNA methyltransferase 1 regulates reelin mRNA expression in mouse primary cortical cultures

2005 ◽  
Vol 102 (5) ◽  
pp. 1749-1754 ◽  
Author(s):  
J. S. Noh ◽  
R. P. Sharma ◽  
M. Veldic ◽  
A. A. Salvacion ◽  
X. Jia ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Dna Methyltransferase ◽  
Dna Methyltransferase 1 ◽  
Cortical Cultures ◽  
Methyltransferase 1
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