Serveur d'exploration sur l'esturgeon

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Toxic effects of PCB126 and TCDD on shortnose sturgeon and Atlantic sturgeon.

Identifieur interne : 000296 ( PubMed/Curation ); précédent : 000295; suivant : 000297

Toxic effects of PCB126 and TCDD on shortnose sturgeon and Atlantic sturgeon.

Auteurs : R Christopher Chambers [États-Unis] ; Dawn D. Davis ; Ehren A. Habeck ; Nirmal K. Roy ; Isaac Wirgin

Source :

RBID : pubmed:22825886

English descriptors

Abstract

Exposure to chemical contaminants is often invoked to explain recruitment failures to populations of sturgeon worldwide, but there is little empirical evidence to support the idea that young sturgeon are sensitive at environmentally relevant concentrations. The authors used shortnose sturgeon (Acipenser brevirostum) and Atlantic sturgeon (Acipenser oxyrinchus) as models to investigate the sensitivities of sturgeon to early-life-stage toxicities from embryonic exposures to graded doses of polychlorinated biphenyl 126 (PCB126) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Survival to hatching of shortnose sturgeon decreased with increasing dose, although the duration of the embryonic period was not significantly altered by exposure in either species. Morphometric features of larvae of both species were affected by dose, including shortening of the body, reduction in head size, reduction in quantity of yolk reserves, and reduction in eye size. Eye development in both species was delayed with increasing dose for both chemicals. The persistence of larvae in a food-free environment decreased inversely with dose in both species, with sharp declines occurring at PCB126 and TCDD doses of ≥1 ppb and ≥0.1 ppb, respectively. Dose-responsive early-life-stage toxicities reported here are among the more sensitive found in fish and occurred at burdens similar to those found in situ in a sympatric bottom-dwelling bony fish in the Hudson River Estuary. The present study is among the first demonstrating the sensitivity of any sturgeon to the hallmark early-life-stage toxicities induced by aryl hydrocarbon receptor agonists.

DOI: 10.1002/etc.1953
PubMed: 22825886

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pubmed:22825886

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<div type="abstract" xml:lang="en">Exposure to chemical contaminants is often invoked to explain recruitment failures to populations of sturgeon worldwide, but there is little empirical evidence to support the idea that young sturgeon are sensitive at environmentally relevant concentrations. The authors used shortnose sturgeon (Acipenser brevirostum) and Atlantic sturgeon (Acipenser oxyrinchus) as models to investigate the sensitivities of sturgeon to early-life-stage toxicities from embryonic exposures to graded doses of polychlorinated biphenyl 126 (PCB126) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Survival to hatching of shortnose sturgeon decreased with increasing dose, although the duration of the embryonic period was not significantly altered by exposure in either species. Morphometric features of larvae of both species were affected by dose, including shortening of the body, reduction in head size, reduction in quantity of yolk reserves, and reduction in eye size. Eye development in both species was delayed with increasing dose for both chemicals. The persistence of larvae in a food-free environment decreased inversely with dose in both species, with sharp declines occurring at PCB126 and TCDD doses of ≥1 ppb and ≥0.1 ppb, respectively. Dose-responsive early-life-stage toxicities reported here are among the more sensitive found in fish and occurred at burdens similar to those found in situ in a sympatric bottom-dwelling bony fish in the Hudson River Estuary. The present study is among the first demonstrating the sensitivity of any sturgeon to the hallmark early-life-stage toxicities induced by aryl hydrocarbon receptor agonists.</div>
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<RefSource>Environ Sci Technol. 2004 Feb 15;38(4):976-83</RefSource>
<PMID Version="1">14998007</PMID>
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<CommentsCorrections RefType="Cites">
<RefSource>Proc Natl Acad Sci U S A. 1997 Dec 9;94(25):13743-8</RefSource>
<PMID Version="1">9391097</PMID>
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<RefSource>Toxicol Sci. 1999 Jan;47(1):40-51</RefSource>
<PMID Version="1">10048152</PMID>
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<CommentsCorrections RefType="Cites">
<RefSource>Environ Sci Technol. 2004 Dec 1;38(23):6300-6</RefSource>
<PMID Version="1">15597885</PMID>
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<RefSource>J Steroid Biochem Mol Biol. 2011 Oct;127(1-2):96-101</RefSource>
<PMID Version="1">21168493</PMID>
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<RefSource>Environ Health Perspect. 2005 Dec;113(12):1675-82</RefSource>
<PMID Version="1">16330346</PMID>
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<PMID Version="1">16936225</PMID>
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<RefSource>J Toxicol Environ Health A. 2007 Sep;70(18):1542-55</RefSource>
<PMID Version="1">17710614</PMID>
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<RefSource>J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2009 Oct;27(4):276-85</RefSource>
<PMID Version="1">19953399</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites">
<RefSource>Aquat Toxicol. 2011 Jul;104(1-2):23-31</RefSource>
<PMID Version="1">21543048</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites">
<RefSource>Mar Environ Res. 2011 May;71(4):257-65</RefSource>
<PMID Version="1">21349578</PMID>
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<RefSource>Aquat Toxicol. 2010 Aug 15;99(2):232-40</RefSource>
<PMID Version="1">20605646</PMID>
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<RefSource>Toxicol Sci. 2003 Nov;76(1):138-50</RefSource>
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<RefSource>Mol Ecol. 2002 Oct;11(10):1885-98</RefSource>
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