Toxic effects of PCB126 and TCDD on shortnose sturgeon and Atlantic sturgeon.
Identifieur interne : 000438 ( Ncbi/Curation ); précédent : 000437; suivant : 000439Toxic 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 WirginSource :
- Environmental toxicology and chemistry [ 1552-8618 ] ; 2012.
English descriptors
- KwdEn :
- MESH :
- chemical , toxicity : Polychlorinated Biphenyls, Polychlorinated Dibenzodioxins, Water Pollutants, Chemical.
- chemistry : Rivers.
- embryology : Fishes.
- growth & development : Fishes, Larva.
- Animals, Environmental Monitoring, Toxicity Tests.
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:22825886Le document en format XML
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<front><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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