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dc.contributor.authorLe, T T Yen
dc.contributor.authorMilen, Nachev
dc.contributor.authorGrabner, Daniel
dc.contributor.authorHendriks, A Jan
dc.contributor.authorPeijnenburg, Willie J G M
dc.contributor.authorSures, Bernd
dc.date.accessioned2021-09-12T18:50:15Z
dc.date.available2021-09-12T18:50:15Z
dc.date.issued2021-08-18
dc.identifier.pmid34426290
dc.identifier.doi10.1016/j.chemosphere.2021.131930
dc.identifier.urihttp://hdl.handle.net/10029/625223
dc.description.abstractA toxicokinetic-toxicodynamic model was constructed to delineate the exposure-response causality. The model could be used: to predict metal accumulation considering the influence of water chemistry and biotic ligand characteristics; to simulate the dynamics of subcellular partitioning considering metabolism, detoxification, and elimination; and to predict chronic toxicity as represented by biomarker responses from the concentration of metals in the fraction of potentially toxic metal. The model was calibrated with data generated from an experiment in which the Zebra mussel Dreissena polymorpha was exposed to Cu at nominal concentrations of 25 and 50 μg/L and with varied Na+ concentrations in water up to 4.0 mmol/L for 24 days. Data used in the calibration included physicochemical conditions of the exposure environment, Cu concentrations in subcellular fractions, and oxidative stress-induced responses, i.e. glutathione-S-transferase activity and lipid peroxidation. The model explained the dynamics of subcellular Cu partitioning and the effect mechanism reasonably well. With a low affinity constant for Na + binding to Cu2+ uptake sites, Na + had limited influence on Cu2+ uptake at low Na+ concentrations in water. Copper was taken up into the metabolically available pool (MAP) at a largely higher rate than into the cellular debris. Similar Cu concentrations were found in these two fractions at low exposure levels, which could be attributed to sequestration pathways (metabolism, detoxification, and elimination) in the MAP. However, such sequestration was inefficient as shown by similar Cu concentrations in detoxified fractions with increasing exposure level accompanied by the increasing Cu concentration in the MAP.en_US
dc.language.isoenen_US
dc.rightsCopyright © 2021 Elsevier Ltd. All rights reserved.
dc.subjectBiomarkersen_US
dc.subjectBiotic ligand modelen_US
dc.subjectBivalvesen_US
dc.subjectChronic toxicityen_US
dc.subjectSubcellular partitioningen_US
dc.subjectToxicokinetic-toxicodynamic modelen_US
dc.titleDelineation of the exposure-response causality chain of chronic copper toxicity to the zebra mussel, Dreissena polymorpha, with a TK-TD model based on concepts of biotic ligand model and subcellular metal partitioning model.en_US
dc.typeArticleen_US
dc.identifier.eissn1879-1298
dc.identifier.journalChemosphere 2022; 286(3):131930 advance online publication (ahead of print)en_US
dc.source.journaltitleChemosphere
dc.source.volume286
dc.source.issuePt 3
dc.source.beginpage131930
dc.source.endpage
dc.source.countryEngland


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