PMID- 9708879
OWN - NLM
STAT- MEDLINE
DCOM- 19981019
LR  - 20190905
IS  - 0340-5761 (Print)
IS  - 0340-5761 (Linking)
VI  - 72
IP  - 7
DP  - 1998 Jun
TI  - Induction of ethoxyresorufin O-deethylase (EROD) and endothelial activation of 
      the heterocyclic amine Trp-P-1 in bird embryo hearts.
PG  - 402-10
AB  - The xenobiotic-metabolizing activity of avian heart was investigated in chicken 
      and Eider duck embryos exposed to aryl hydrocarbon (Ah) receptor agonists in ovo. 
      Both beta-naphthoflavone (BNF) and 3,3',4,4',5-pentachlorobiphenyl (PCB 126) 
      induced 7-ethoxyresorufin O-deethylase (EROD) activities in chicken embryo hearts 
      whereas Eider duck embryos only responded to BNF. The differential responses of 
      chicken and Eider duck embryos were used to examine the involvement of Ah 
      receptor-mediated enzyme induction in the activation of the environmental and 
      food mutagen 3-amino- 1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1). As 
      determined by light microscopic autoradiography, there was a highly selective 
      binding of non-extractable 3H-Trp-P-1-derived radioactivity in endothelial cells 
      of large vessels and capillaries in hearts of BNF- and PCB 126-treated chicken 
      embryos. No binding occurred at these sites in vehicle-treated controls. There 
      was also a strong endothelial binding of 3H-Trp-P-1 in hearts of BNF-treated 
      Eider duck embryos whereas no binding occurred in hearts of PCB 126-treated Eider 
      duck embryos. A positive correlation between induction of EROD activity and 
      covalent binding of 3H-Trp-P-1 to protein in heart homogenates from BNF- and PCB 
      126-treated chicken and Eider duck embryos was also observed. The results suggest 
      a cytochrome P450 1A (CYP1A)-mediated activation of Trp-P-1 in avian heart 
      endothelial cells although involvement of other Ah receptor-regulated enzymes is 
      also possible. We propose that heart endothelial cells may be targets for 
      bioactivation and toxicity of environmental contaminants in birds exposed to Ah 
      receptor agonists.
FAU - Annas, A
AU  - Annas A
AD  - Department of Pharmaceutical Biosciences, Uppsala University, Sweden.
FAU - Brunstrom, B
AU  - Brunstrom B
FAU - Brandt, I
AU  - Brandt I
FAU - Brittebo, E B
AU  - Brittebo EB
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Arch Toxicol
JT  - Archives of toxicology
JID - 0417615
RN  - 0 (Carbolines)
RN  - EC 1.14.14.1 (Cytochrome P-450 CYP1A1)
RN  - LAH2R5Z22D (3-amino-1,4-dimethyl-5H-pyrido(4,3-b)indole)
SB  - IM
MH  - Animals
MH  - Autoradiography
MH  - Carbolines/*pharmacology
MH  - Chick Embryo
MH  - Cytochrome P-450 CYP1A1/*biosynthesis
MH  - Ducks/embryology
MH  - Endothelium/drug effects
MH  - Enzyme Induction
MH  - Heart/*drug effects/embryology
MH  - Myocardium/enzymology
EDAT- 1998/08/26 00:00
MHDA- 1998/08/26 00:01
CRDT- 1998/08/26 00:00
PHST- 1998/08/26 00:00 [pubmed]
PHST- 1998/08/26 00:01 [medline]
PHST- 1998/08/26 00:00 [entrez]
AID - 10.1007/s002040050520 [doi]
PST - ppublish
SO  - Arch Toxicol. 1998 Jun;72(7):402-10. doi: 10.1007/s002040050520.