Oxidative stress in Lake Sturgeon (Acipenser fulvescens) orally exposed to 2,3,7,8-tetrachlorodibenzofuran
Identifieur interne : 001991 ( Main/Exploration ); précédent : 001990; suivant : 001992Oxidative stress in Lake Sturgeon (Acipenser fulvescens) orally exposed to 2,3,7,8-tetrachlorodibenzofuran
Auteurs : V. P. Palace [Canada] ; T. A. Dick [Canada] ; S. B. Brown [Canada] ; C. L. Baron [Canada] ; J. F. Klaverkamp [Canada]Source :
- Aquatic toxicology [ 0166-445X ] ; 1996.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Copyright (c) 1996 Elsevier Science B.V. All rights reserved. Juvenile lake sturgeon were orally dosed with gelatin containing nominal concentrations of 0, 0.16 or 1.6 ng [3H]-2,3,7,8-tetrachlorodibenzofuran (TCDF) kg-1 fish weight. Liver, kidney and blood were collected 10 and 27 days after exposure. Phase I mixed-function oxidase (MFO) and Phase II (glucuronyltransferase) enzyme activities were determined in liver. Concentrations of non-enzymatic (tocopherol, retinoids) and enzymatic (superoxide dismutase, catalase, glutathione peroxidase) antioxidant parameters were also quantified in liver and kidney. TCDF concentrations were elevated in liver and kidney of both dose groups at 10 and 27 days. Lower tissue concentrations of TCDF at 27 days, compared with 10 day exposures, as well as the presence of polar metabolites in bile, may indicate rapid metabolism and clearance of the contaminant. MFO enzyme activity, measured as ethoxyresorufin-O-de-ethylase (EROD), was induced in liver with activity at the two sample periods reflecting the TCDF concentrations. Greater concentrations of hepatic lipid peroxides in both dose groups, indicate that oxidative stress was produced by contaminant exposure and/or induced metabolism enzyme activity.
Affiliations:
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P." last="Palace">V. P. Palace</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>University of Manitoba</s1><s2>Winnipeg, Man. R3T 2N6</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Winnipeg</settlement><region type="state">Manitoba</region></placeName><orgName type="university">Université du Manitoba</orgName></affiliation></author><author><name sortKey="Dick, T A" sort="Dick, T A" uniqKey="Dick T" first="T. A." last="Dick">T. A. Dick</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>University of Manitoba</s1><s2>Winnipeg, Man. 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R3T 2N6</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Aquatic toxicology</title><title level="j" type="abbreviated">Aquat. toxicol.</title><idno type="ISSN">0166-445X</idno><imprint><date when="1996">1996</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Aquatic toxicology</title><title level="j" type="abbreviated">Aquat. toxicol.</title><idno type="ISSN">0166-445X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antioxidant</term><term>Biological accumulation</term><term>Effluent</term><term>Enzymatic activity</term><term>Lipophilic compound</term><term>Metabolism</term><term>Oxidative stress</term><term>Paper mill</term><term>Toxicity</term><term>Water pollution</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Pollution eau</term><term>Effluent</term><term>Papeterie</term><term>Accumulation biologique</term><term>Composé lipophile</term><term>Toxicité</term><term>Stress oxydatif</term><term>Activité enzymatique</term><term>Métabolisme</term><term>Antioxydant</term><term>Acipenser fulvescens</term><term>Acipenseridae</term><term>2,3,7,8-tetrachlorodibenzofuran</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Copyright (c) 1996 Elsevier Science B.V. All rights reserved. Juvenile lake sturgeon were orally dosed with gelatin containing nominal concentrations of 0, 0.16 or 1.6 ng [<sup>3</sup>H]-2,3,7,8-tetrachlorodibenzofuran (TCDF) kg<sup>-1</sup> fish weight. Liver, kidney and blood were collected 10 and 27 days after exposure. Phase I mixed-function oxidase (MFO) and Phase II (glucuronyltransferase) enzyme activities were determined in liver. Concentrations of non-enzymatic (tocopherol, retinoids) and enzymatic (superoxide dismutase, catalase, glutathione peroxidase) antioxidant parameters were also quantified in liver and kidney. TCDF concentrations were elevated in liver and kidney of both dose groups at 10 and 27 days. Lower tissue concentrations of TCDF at 27 days, compared with 10 day exposures, as well as the presence of polar metabolites in bile, may indicate rapid metabolism and clearance of the contaminant. MFO enzyme activity, measured as ethoxyresorufin-O-de-ethylase (EROD), was induced in liver with activity at the two sample periods reflecting the TCDF concentrations. Greater concentrations of hepatic lipid peroxides in both dose groups, indicate that oxidative stress was produced by contaminant exposure and/or induced metabolism enzyme activity.</div></front></TEI><affiliations><list><country><li>Canada</li></country><region><li>Manitoba</li></region><settlement><li>Winnipeg</li></settlement><orgName><li>Université du Manitoba</li></orgName></list><tree><country name="Canada"><region name="Manitoba"><name sortKey="Palace, V P" sort="Palace, V P" uniqKey="Palace V" first="V. P." last="Palace">V. P. Palace</name></region><name sortKey="Baron, C L" sort="Baron, C L" uniqKey="Baron C" first="C. L." last="Baron">C. L. Baron</name><name sortKey="Brown, S B" sort="Brown, S B" uniqKey="Brown S" first="S. B." last="Brown">S. B. Brown</name><name sortKey="Dick, T A" sort="Dick, T A" uniqKey="Dick T" first="T. A." last="Dick">T. A. Dick</name><name sortKey="Klaverkamp, J F" sort="Klaverkamp, J F" uniqKey="Klaverkamp J" first="J. F." last="Klaverkamp">J. F. Klaverkamp</name><name sortKey="Klaverkamp, J F" sort="Klaverkamp, J F" uniqKey="Klaverkamp J" first="J. F." last="Klaverkamp">J. F. Klaverkamp</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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