Ah receptor involvement in mediation of pyruvate carboxylase levels and activity in mice given 2,3,7,8-tetrachlorodibenzo-p-dioxin

1995 ◽  
Vol 10 (2) ◽  
pp. 103-109 ◽  
Author(s):  
Byung-Woo Ryu ◽  
Shukla Roy ◽  
Barney R. Sparrow ◽  
Daniel P. Selivonchick ◽  
Henry W. Schaup
Keyword(s):  
Pyruvate Carboxylase ◽  
Ah Receptor ◽  
Tetrachlorodibenzo P Dioxin

scholarly journals Photoaffinity labeling of the nuclear Ah receptor from mouse Hepa 1c1c7 cells using 2,3,7,8-[3H]tetrachlorodibenzo-p-dioxin

1989 ◽  
Vol 264 (31) ◽  
pp. 18463-18471
Author(s):  
J P Landers ◽  
J Piskorska-Pliszczynska ◽  
T Zacharewski ◽  
N J Bunce ◽  
S Safe
Keyword(s):  
Photoaffinity Labeling ◽  
Ah Receptor ◽  
Tetrachlorodibenzo P Dioxin

Inhibition of 3T3-L1 adipose differentiation by 2,3,7,8-tetrachlorodibenzo-p-dioxin

1995 ◽  
Vol 108 (1) ◽  
pp. 395-402 ◽  
Author(s):  
M. Phillips ◽  
E. Enan ◽  
P.C. Liu ◽  
F. Matsumura
Keyword(s):  
Northern Blotting ◽  
Ah Receptor ◽  
Reporter Construct ◽  
Fat Cell ◽  
Camp Signaling Pathway ◽  
Adipose Differentiation ◽  
Tetrachlorodibenzo P Dioxin ◽  
Oil Red O Staining ◽  
Oil Red O ◽  
Do So

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-induced toxicity is particularly striking in adipose tissue, where it causes severe wasting. This phenomenon suggests that TCDD could have effects on adipocyte differentiation, now demonstrated using 3T3-L1 cells as a model system. When cells were treated with 10 nM TCDD before differentiation or during the first two days of induction in the presence of dexamethasone (dex) and isobutylmethylxanthine (IBMX), a reduction occurred in the number of fat cell colonies measured 7–10 days later by Oil Red O staining. Northern blotting showed an accompanying reduction in amounts of mRNA encoding several adipocyte markers. In contrast, when TCDD was added after differentiation, it had no effect on the maintenance of the adipose phenotype. Dose-response and structure-activity relationships were consistent with a process mediated by interaction of TCDD with the Ah receptor. The possibility that TCDD acts by inhibiting the signaling pathways activated by dex and IBMX was investigated. TCDD did not interfere with glucocorticoid-inducible transcription as judged by the unimpaired responsiveness of a transfected reporter construct. Treatment of cells with TCDD augmented the increase in protein kinase A (PKA) activity elicited by either IBMX or forskolin; therefore, if TCDD disrupts the cAMP signaling pathway, it must do so at a step after activation of PKA.

Ah Receptor and ARNT Protein and mRNA Concentrations in Rat Prostate: Effects of Stage of Development and 2,3,7,8-Tetrachlorodibenzo-p-Dioxin Treatment

1999 ◽  
Vol 155 (2) ◽  
pp. 177-189 ◽  
Author(s):  
Rebecca J. Sommer ◽  
Katherine Marks Sojka ◽  
Richard S. Pollenz ◽  
Paul S. Cooke ◽  
Richard E. Peterson
Keyword(s):  
Ah Receptor ◽  
Stage Of Development ◽  
Tetrachlorodibenzo P Dioxin ◽  
Rat Prostate

Ah receptor in spleen of rodent and primate species: detection by binding of 2,3,7,8-tetrachlorodibenzo-p-dioxin

1989 ◽  
Vol 67 (6) ◽  
pp. 594-600 ◽  
Author(s):  
Eve A. Roberts ◽  
Lynn M. Vella ◽  
Cheryl L. Golas ◽  
Leslie A. Dafoe ◽  
Allan B. Okey
Keyword(s):  
Rhesus Monkeys ◽  
Specific Binding ◽  
Velocity Sedimentation ◽  
Primate Species ◽  
Ah Receptor ◽  
Sprague Dawley ◽  
Wasting Syndrome ◽  
Specific Organ ◽  
Tetrachlorodibenzo P Dioxin ◽  
Tcdd Toxicity

In many species systemic toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is manifested by a generalized wasting syndrome accompanied by a variety of specific organ changes including atrophy of the thymus and spleen. TCDD toxicity in most tissues is thought to be mediated by the Ah receptor. Although the spleen is a prime target for TCDD toxicity, the possible presence of Ah receptor in the spleen has not previously been investigated. Specific binding of [3H]TCDD to Ah receptor in spleen cytosols was assessed by velocity sedimentation on sucrose gradients. Ah receptor was detected in spleen cytosols from adult Rhesus monkeys (mean ± SEM, 36 ± 8 fmol/mg cytosol protein), fetal Rhesus monkeys (9 ± 6), Sprague–Dawley rats (20 ± 5), C57BL/6J mice (18 ± 2), New Zealand white rabbits (19 ± 2), and Hartley guinea pigs (15 ± 2). Ah receptor was not detectable in spleen cytosol from genetically "nonresponsive" DBA/2J mice or from Golden Syrian hamsters, a species resistant to toxicity of TCDD. Molecular properties of Ah receptor from spleen were similar to those of the receptor from liver of the same species. The high Ah receptor content in spleen cytosols from those species that are most susceptible to TCDD toxicity is consistent with the view that the Ah receptor mediates TCDD toxicity in spleen as well as in other tissues.Key words: Ah receptor, 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin, immunotoxicity, spleen.

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