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Titolo:
Induction and suppression of cytochrome P450 1A by 3,3 ',4,4 ',5-pentachlorobiphenyl and its relationship to oxidative stress in the marine fish scup(Stenotomus chrysops)
Autore:
Schlezinger, JJ; Stegeman, JJ;
Indirizzi:
Woods Hole Oceanog Inst, Dept Biol, Woods Hole, MA 02543 USA Woods Hole Oceanog Inst Woods Hole MA USA 02543 Woods Hole, MA 02543 USA
Titolo Testata:
AQUATIC TOXICOLOGY
fascicolo: 2, volume: 52, anno: 2001,
pagine: 101 - 115
SICI:
0166-445X(200104)52:2<101:IASOCP>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
POLYCHLORINATED-BIPHENYLS PCBS; TROUT ONCORHYNCHUS-MYKISS; RAINBOW-TROUT; HYDROCARBON RECEPTOR; WINTER FLOUNDER; TOXICOLOGICAL ASSESSMENT; METABOLISM INVIVO; CROSS-REACTIVITY; TELEOST FISH; AH RECEPTOR;
Keywords:
cytochrome P450 1A; 3,3 ',4,4 ',5-pentachlorobiphenyl; oxidative stress; Stenotomus chrysops;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Citazioni:
61
Recensione:
Indirizzi per estratti:
Indirizzo: Stegeman, JJ Woods Hole Oceanog Inst, Dept Biol, Redfield 342,MS 32, WoodsHole, MA 02543 USA Woods Hole Oceanog Inst Redfield 342,MS 32 Woods Hole MA USA 02543
Citazione:
J.J. Schlezinger e J.J. Stegeman, "Induction and suppression of cytochrome P450 1A by 3,3 ',4,4 ',5-pentachlorobiphenyl and its relationship to oxidative stress in the marine fish scup(Stenotomus chrysops)", AQUAT TOX, 52(2), 2001, pp. 101-115

Abstract

The planar polychlorinated biphenyl (PCB) 3,3',4,4'-tetrachlorobiphenyl (TCB) causes dose-dependent induction and post-transcriptional suppression ofhepatic cytochrome P450 1A (CYP1A) in the marine teleost scup (Stenotomus chrysops). That suppression is linked to inhibition and oxidative inactivation of CYP1A by TCB. Other planar PCBs, including 3,3',4,4',5-pentachlorobiphenyl (PeCB), inactivate scup CYP1A in vitro leading us to hypothesize that PeCB also will suppress CYP1A in vivo. We examined induction and suppression of CYP1A by PeCB in scup, as related to oxidative stress. PeCB at a lowdose (0.01 mg/kg) induced hepatic microsomal spectral P450 and CYP1A protein and catalytic activities (ethoxyresorufin o-deethylase (EROD) and methoxyresorufin o-demethylase (MROD)) over an 18 day period. A high dose (1 mg PeCB/kg) only minimally induced hepatic spectral P450 and CYP1A content, andEROD and MROD rates remained at control levels at all sampling times, while CYP1A mRNA expression was induced strongly (up to 35-fold) at both doses. High dose PeCB had minimal effects on content of P450A (a CYP3A protein), P450B (a CYP2B-like protein) and cytochrome b5 in scup liver, suggesting that the suppression was specific for CYP1A. High dose PeCB suppressed EROD but not CYP1A protein in the kidney but did not strongly suppress either CYP1A or EROD in the heart or gill. PeCB stimulated ROS production (oxidation of dihydroethidium) by liver microsomes from the low dose but not the high dose fish, and the rate of PeCB-stimulated ROS production was correlated with EROD activity (r(2) = 0.641, P < 0.0005). Oxidative stress, indicated byincreased levels of catalase, glutathione peroxidase, glutathione reductase and superoxide dismutase activities, was stimulated in the liver by low dose but not high dose PeCB. The results support a hypothesis that many PHAHcan inactivate teleost CYP1A in vivo, and that CYP1A is a source of ROS. However, there appears to be a complex balance between the effects of PeCB on the levels of active CYP1A, ROS release and oxidative stress. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 00:24:30