Biochemical effects of 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) and related compounds on the central nervous system

2,3,7,8-Tetrachlorodibenzo- p-dioxin (TCDD) and related compounds are an important class of environmental contaminants which induce several types of biochemical alterations. Their effects have been most thoroughly characterized in the liver, especially regarding the Ah receptor-mediated induction of...

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Bibliographic Details
Published in:International Journal of Biochemistry and Cell Biology 1995-05, Vol.27 (5), p.443-455
Main Authors: Unkila, Mikko, Pohjanvirta, Raimo, Tuomisto, Jouko
Format: Article
Language:English
Subjects:
2,3,7,8-Tetrachlorodibenzo- p-dioxin
Ah receptor
ah receptors
Animals
catecholamines
central nervous system
Central Nervous System - drug effects
chemical structure
CNS
CYP1A1
cytochrome P-450
Dioxin
dioxins
gene induction
Humans
induction
lethal dose
mammals
Molecular Structure
Neurotoxicity
neurotoxins
oxidoreductases
polychlorinated biphenyls
Polychlorinated Dibenzodioxins - analogs & derivatives
Polychlorinated Dibenzodioxins - toxicity
receptors
Serotonin
structure
TCDD
Tryptophan
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Summary:2,3,7,8-Tetrachlorodibenzo- p-dioxin (TCDD) and related compounds are an important class of environmental contaminants which induce several types of biochemical alterations. Their effects have been most thoroughly characterized in the liver, especially regarding the Ah receptor-mediated induction of xenobiotic metabolizing enzymes. The behavioral signs exhibited by animals exposed to TCDD (progressive anorexia and body weight loss) suggest a role for the central nervous system (CNS) in TCDD toxicity. At lethal doses, TCDD affects the metabolism of serotonin, a neurotransmitter able to modulate food intake in the brain. This effect is associated with an elevated concentration of free tryptophan in the plasma. There does not appear to be any major changes in catecholaminergic neurotransmitter systems in TCDD-treated rats. Cytochrome P-450 related enzyme activities are induced by TCDD in the brain. As is the case in the liver, this induction does not correlate with susceptibility to TCDD lethality in rats. The involvement of the CNS in TCDD toxicity is still obscure. Elucidation of this role as well as the mechanism of TCDD-induced wasting may well advance our understanding of the regulation of food intake and body weight
ISSN:1357-2725
1878-5875
DOI:10.1016/1357-2725(95)00023-I