PMID- 10967401
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20191120
IS  - 1879-1514 (Electronic)
IS  - 0166-445X (Linking)
VI  - 50
IP  - 4
DP  - 2000 Oct 1
TI  - Effect of a dioxin-like PCB (CB 126) on the biotransformation and genotoxicity of 
      benzo.
PG  - 403-415
AB  - Two experiments were performed to study the interaction between benzo[a]pyrene 
      (BaP) and the planar, dioxin-like PCB congener 3,3',4,4',5-pentachlorobiphenyl 
      (CB 126) in the flatfish dab (Limanda limanda). The first experiment involved 
      four groups. Group I was treated with 10 microg/kg CB 126, group II was treated with 
      2 mg/kg BaP, group III was first treated with 10 microg/kg CB 126 and exposed to 2 
      mg/kg BaP 6 days later, and group IV was a control group. The second experiment 
      was similar, except that the BaP dosage level was increased to 50 mg/kg. 
      Pre-treatment with 10 microg/kg of CB 126 always caused the induction of hepatic 
      cytochrome P450 1A (CYP1A), as measured by significant increases of the model 
      reaction 7-ethoxyresorufin-O-deethylase (EROD) in microsomal preparations. 
      Treatment of dab with BaP caused a significant EROD induction at the 50 mg/kg, 
      but not at the 2 mg/kg level. Concurrent with EROD induction by either CB 126 or 
      50 mg/kg BaP, was a significant change in the biliary metabolite pattern in 
      favour of 1-hydroxybenzo[a]pyrene and 3-hydroxybenzo[a]pyrene and towards a lower 
      fraction of the procarcinogen BaP-7,8-dihydrodiol (7,8-DIOL). Pre-treatment with 
      CB 126 did not cause an increase of hepatic BaP DNA adducts formed after 
      treatment with either 2 or 50 mg/kg BaP. Glutathione S-transferase (GST) 
      activities remained also unaffected by any of the treatments. The results of this 
      study suggest that the pattern of BaP metabolites in bile depends on the level of 
      CYP1A induction. Moreover, the concurrence of a potent CYP1A inducer and BaP does 
      not necessarily lead to an increase in DNA adduct levels in liver tissue. The 
      observation that the level of 7,8-DIOL is decreased despite a higher (CYP1A 
      mediated) EROD activity explains, at least in part, the lack of induction of DNA 
      adducts.
FAU - van Schanke A
AU  - van Schanke A
AD  - Department of Marine Biogeochemistry and Toxicology, Netherlands Institute for 
      Sea Research (NIOZ), PO Box 59, 1790 AB, Den Burg Texel, The Netherlands
FAU - Boon, JP
AU  - Boon JP
FAU - Aardoom, Y
AU  - Aardoom Y
FAU - van Leest A
AU  - van Leest A
FAU - van Schooten FJ
AU  - van Schooten FJ
FAU - Maas, L
AU  - Maas L
FAU - van den Berg M
AU  - van den Berg M
FAU - Everaarts, JM
AU  - Everaarts JM
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Aquat Toxicol
JT  - Aquatic toxicology (Amsterdam, Netherlands)
JID - 8500246
EDAT- 2000/09/01 00:00
MHDA- 2000/09/01 00:01
CRDT- 2000/09/01 00:00
PHST- 2000/09/01 00:00 [pubmed]
PHST- 2000/09/01 00:01 [medline]
PHST- 2000/09/01 00:00 [entrez]
AID - S0166445X00000862 [pii]
AID - 10.1016/s0166-445x(00)00086-2 [doi]
PST - ppublish
SO  - Aquat Toxicol. 2000 Oct 1;50(4):403-415. doi: 10.1016/s0166-445x(00)00086-2.