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Weber, L.W.D. ; Stahl, B.U. ; Rozman, K.K.

Are Serotonergic Mechanisms Involved in the Acute Toxicity of Chlorinated Dibenzo-p-dioxins ( CDDs)?.

Chemosphere 25, 161-164 (1992)
DOI
Open Access Gold möglich sobald Verlagsversion bei der ZB eingereicht worden ist.
The mechanism of CDD-induced appetite suppression was studied in male Sprague-Dawley rats. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) served as the model compound; additional experiments were performed using higher chlorinated CDDs (penta-, hexa-, hepta-, and a mixture) with substituents in the biologically crucial 2-, 3-, 7-, and 8-positions. All homologues, plus their equipotent mixture, led to an increase of plasma and brain tryptophan (TRP) levels and concomitantly serotonin (5-HT) turnover, in the very same dose range where acute toxicity occurred. The reason for elevated TRP levels was an inhibition of the activity of tryptophan 2,3-dioxygenase (TdO) in the livers of treated animals. A direct effect of TCDD on the central nervous system (CNS) was ruled out. Depletion of CNS 5-HT stores by administration of 5,7-dihydroxytryptamine (5,7-dHT) did not influence the TCDD-induced appetite suppression, and thus it was concluded that 5-HT causes aphagia by a peripheral mechanism. Based on the similarity of symptoms caused by CDDs on the one hand, and tumor necrosis factor (TNF) on the other hand, a mechanism of action is proposed where CDDs render the organism non-responsive to glucocorticoid receptor-mediated stimuli, locking the activities of several key enzymes of intermediary metabolism to low levels which do not allow the organism to respond appropriately to appetite suppression and hypoglycemia.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Sprache englisch
Veröffentlichungsjahr 1992
HGF-Berichtsjahr 0
ISSN (print) / ISBN 0045-6535
e-ISSN 1879-1298
Zeitschrift Chemosphere
Quellenangaben Band: 25, Heft: 1-2, Seiten: 161-164 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort Kidlington, Oxford
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Toxicology and Pharmacology (TOX)
DOI 10.1016/0045-6535(92)90503-J
Erfassungsdatum 1992-12-31
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