Relevant bibliographies by topics / Toxicodynamie

Academic literature on the topic 'Toxicodynamie'

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Published: 22 June 2023

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Journal articles on the topic "Toxicodynamie"

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Kasteel, Emma E. J., Sandra M. Nijmeijer, Keyvin Darney, Leonie S. Lautz, Jean Lou C. M. Dorne, Nynke I. Kramer, and Remco H. S. Westerink. "Acetylcholinesterase inhibition in electric eel and human donor blood: an in vitro approach to investigate interspecies differences and human variability in toxicodynamics." Archives of Toxicology 94, no. 12 (October 10, 2020): 4055–65. http://dx.doi.org/10.1007/s00204-020-02927-8.

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Abstract In chemical risk assessment, default uncertainty factors are used to account for interspecies and interindividual differences, and differences in toxicokinetics and toxicodynamics herein. However, these default factors come with little scientific support. Therefore, our aim was to develop an in vitro method, using acetylcholinesterase (AChE) inhibition as a proof of principle, to assess both interspecies and interindividual differences in toxicodynamics. Electric eel enzyme and human blood of 20 different donors (12 men/8 women) were exposed to eight different compounds (chlorpyrifos, chlorpyrifos-oxon, phosmet, phosmet-oxon, diazinon, diazinon-oxon, pirimicarb, rivastigmine) and inhibition of AChE was measured using the Ellman method. The organophosphate parent compounds, chlorpyrifos, phosmet and diazinon, did not show inhibition of AChE. All other compounds showed concentration-dependent inhibition of AChE, with IC50s in human blood ranging from 0.2–29 µM and IC20s ranging from 0.1–18 µM, indicating that AChE is inhibited at concentrations relevant to the in vivo human situation. The oxon analogues were more potent inhibitors of electric eel AChE compared to human AChE. The opposite was true for carbamates, pointing towards interspecies differences for AChE inhibition. Human interindividual variability was low and ranged from 5–25%, depending on the concentration. This study provides a reliable in vitro method for assessing human variability in AChE toxicodynamics. The data suggest that the default uncertainty factor of ~ 3.16 may overestimate human variability for this toxicity endpoint, implying that specific toxicodynamic-related adjustment factors can support quantitative in vitro to in vivo extrapolations that link kinetic and dynamic data to improve chemical risk assessment.
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Boak, Lauren M., Craig R. Rayner, M. Lindsay Grayson, David L. Paterson, Denis Spelman, Sharmila Khumra, Blair Capitano, et al. "Clinical Population Pharmacokinetics and Toxicodynamics of Linezolid." Antimicrobial Agents and Chemotherapy 58, no. 4 (February 10, 2014): 2334–43. http://dx.doi.org/10.1128/aac.01885-13.

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ABSTRACTThrombocytopenia is a common side effect of linezolid, an oxazolidinone antibiotic often used to treat multidrug-resistant Gram-positive bacterial infections. Various risk factors have been suggested, including linezolid dose and duration of therapy, baseline platelet counts, and renal dysfunction; still, the mechanisms behind this potentially treatment-limiting toxicity are largely unknown. A clinical study was conducted to investigate the relationship between linezolid pharmacokinetics and toxicodynamics and inform strategies to prevent and manage linezolid-associated toxicity. Forty-one patients received 42 separate treatment courses of linezolid (600 mg every 12 h). A new mechanism-based, population pharmacokinetic/toxicodynamic model was developed to describe the time course of plasma linezolid concentrations and platelets. A linezolid concentration of 8.06 mg/liter (101% between-patient variability) inhibited the synthesis of platelet precursor cells by 50%. Simulations predicted treatment durations of 5 and 7 days to carry a substantially lower risk than 10- to 28-day therapy for platelet nadirs of <100 ×109/liter. The risk for toxicity did not differ noticeably between 14 and 28 days of therapy and was significantly higher for patients with lower baseline platelet counts. Due to the increased risk of toxicity after longer durations of linezolid therapy and large between-patient variability, close monitoring of patients for development of toxicity is important. Dose individualization based on plasma linezolid concentration profiles and platelet counts should be considered to minimize linezolid-associated thrombocytopenia. Overall, oxazolidinone therapy over 5 to 7 days even at relatively high doses was predicted to be as safe as 10-day therapy of 600 mg linezolid every 12 h.
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Blanchette, Alexander D., Sarah D. Burnett, Fabian A. Grimm, Ivan Rusyn, and Weihsueh A. Chiu. "A Bayesian Method for Population-wide Cardiotoxicity Hazard and Risk Characterization Using an In Vitro Human Model." Toxicological Sciences 178, no. 2 (October 20, 2020): 391–403. http://dx.doi.org/10.1093/toxsci/kfaa151.

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Abstract Human induced pluripotent stem cell (iPSC)-derived cardiomyocytes are an established model for testing potential chemical hazards. Interindividual variability in toxicodynamic sensitivity has also been demonstrated in vitro; however, quantitative characterization of the population-wide variability has not been fully explored. We sought to develop a method to address this gap by combining a population-based iPSC-derived cardiomyocyte model with Bayesian concentration-response modeling. A total of 136 compounds, including 54 pharmaceuticals and 82 environmental chemicals, were tested in iPSC-derived cardiomyocytes from 43 nondiseased humans. Hierarchical Bayesian population concentration-response modeling was conducted for 5 phenotypes reflecting cardiomyocyte function or viability. Toxicodynamic variability was quantified through the derivation of chemical- and phenotype-specific variability factors. Toxicokinetic modeling was used for probabilistic in vitro-to-in vivo extrapolation to derive population-wide margins of safety for pharmaceuticals and margins of exposure for environmental chemicals. Pharmaceuticals were found to be active across all phenotypes. Over half of tested environmental chemicals showed activity in at least one phenotype, most commonly positive chronotropy. Toxicodynamic variability factor estimates for the functional phenotypes were greater than those for cell viability, usually exceeding the generally assumed default of approximately 3. Population variability-based margins of safety for pharmaceuticals were correctly predicted to be relatively narrow, including some below 10; however, margins of exposure for environmental chemicals, based on population exposure estimates, generally exceeded 1000, suggesting they pose little risk at current general population exposures even to sensitive subpopulations. Overall, this study demonstrates how a high-throughput, human population-based, in vitro-in silico model can be used to characterize toxicodynamic population variability in cardiotoxic risk.
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Kavlock, Robert J., and Gabriel L. Plaa. "Session summary: toxicodynamic interactive mechanisms." Toxicology 105, no. 2-3 (December 1995): 235–36. http://dx.doi.org/10.1016/0300-483x(95)03218-5.

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Ashauer, Roman, and Colin Brown. "TOXICODYNAMIC ASSUMPTIONS IN ECOTOXICOLOGICAL HAZARD MODELS." Environmental Toxicology and Chemistry preprint, no. 2008 (2007): 1. http://dx.doi.org/10.1897/07-642.

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Ashauer, Roman, and Colin D. Brown. "TOXICODYNAMIC ASSUMPTIONS IN ECOTOXICOLOGICAL HAZARD MODELS." Environmental Toxicology and Chemistry 27, no. 8 (2008): 1817. http://dx.doi.org/10.1897/07-642.1.

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Serkova, Natalie J., and Uwe Christians. "Biomarkers for Toxicodynamic Monitoring of Immunosuppressants." Therapeutic Drug Monitoring 27, no. 6 (December 2005): 733–37. http://dx.doi.org/10.1097/01.ftd.0000179846.30342.65.

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Gots, Ronald E., and Suellen W. Pirages. "Multiple Chemical Sensitivities: Psychogenic or Toxicodynamic Origins." International Journal of Toxicology 18, no. 6 (November 1999): 393–400. http://dx.doi.org/10.1080/109158199225107.

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The multiple chemical sensitivity (MCS) phenomenon can cause significant dysfunction and symptomatology and presents a difficult challenge for patient management. Central to the MCS debate is whether this phenomenon results from a primary emotional response to perceived chemical exposures or from pathological interactions between chemicals and biological systems. Those who believe the latter argue that toxic interactions result in physiological impairment and that subsequent emotional problems derive from such impairment. Distinguishing between psychogenic (emotional) or a toxicodynamic (chemical toxicity) origin is essential to the medical management of an MCS patient. A psychogenic basis requires treatment with appropriate behavioral therapies; in contrast, a belief in a strictly toxicodynamic etiology argues for avoidance and often precludes treatments that address the psychological responses. Current scientific evidence strongly suggests that behavioral or psychogenic explanations predominate for reported MCS symptoms. Acceptance of a purely toxic origination (i.e., pathological abnormalities result from a low level chemical exposure) defies known toxicological and medical principles; whereas psychogenic explanations are consistent with these principles. Because symptoms are the end points of many diseases with many causes, both physical and emotional, modern medicine is charged with and expected to consider both when treating MCS patients. The argument can be made that insufficient information exists about the causal nature of many diseases, and future research may provide support for a strict toxicodynamic cause. However, the practice of medicine must be based upon current knowledge, not future possibilities. Proper care of MCS patients requires identifying the existence of both psychological and organic pathological dysfunction. The rejection of a psychological aspect of the MCS phenomenon and appropriate behavioral treatments is both illogical and detrimental to MCS sufferers.
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Reeves, Andrew L. "Beryllium: Toxicological Research of the Last Decade." Journal of the American College of Toxicology 8, no. 7 (December 1989): 1307–13. http://dx.doi.org/10.3109/10915818909009122.

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Danilov-Danilyan, V. I., and O. M. Rozental. "Logistic Model of Population Toxicodynamics." Water Resources 49, no. 2 (March 27, 2022): 231–39. http://dx.doi.org/10.1134/s0097807822020038.

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Abstract The effect of pollutant in water on a population of aquatic organisms as a function of exposure time is studied. Natural assumptions are formulated regarding the character of this process, primarily, the linear relationship between the rate of decrease in the population, on the one hand, and the population size and the number of organisms killed by intoxication, on the other hand. The formulated assumptions are used to construct a model of population toxicodynamics, which describes the kinetics of suppression of the population by a logistic function. The results of model calculations are shown to agree with the available experimental data, thus justifying the formulated assumptions regarding the character of the intoxication process. An extension of the model is proposed through the incorporation of the dependence of the result of intoxication on pollutant concentration by the well-known Haber’s formula. The developed model was used to propose an equation of regulated toxicodynamics for organization of water use without violation of the regime of natural functioning of ecosystems. The obtained specification of the notions of the mechanisms of intoxication process is necessary for the substantiation of hygienic standards on the concentration of chemicals in water, forecasts of biodiversity, and the choice of measures for supporting weak components of trophic chains in aquatic ecosystems.
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Dissertations / Theses on the topic "Toxicodynamie"

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Mit, Corentin. "Modélisation mécaniste de la dynamique de biomarqueurs chez les poissons téléostéens : lien entre exposition et effetsprécoces." Electronic Thesis or Diss., Paris, AgroParisTech, 2023. http://www.theses.fr/2023AGPT0001.

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Les biomarqueurs sont des outils d'un grand intérêt mis en oeuvre pour établir un diagnostic de risque environnemental pour les écosystèmes aquatiques. Néanmoins, la mesure de ces marqueurs sub-individuels présentent encore certaines limitations pour l'évaluation de la qualité des écosystèmes, parmi lesquelles la caractérisation des dynamiques parfois complexes de réponses de ces effets non-léthaux en fonction du temps ou de la dose ou encore l'extrapolation des réponses d'une échelle d'organisation biologique à une autre. Une des solutions semblant prometteuses pour caractériser la dynamique de ces réponses dans une optique de changement d’échelle serait d’intégrer les biomarqueurs à des modèles mécanistiques permettant de prédire cette dynamique et d’expliquer les mécanismes sous-jacents à l’apparition des effets. Ainsi, ce travail de thèse propose de construire des modèles mécanistiques de toxicocinétique et toxicodynamie à base physiologique (PBTK-TD) pour mieux caractériser et mieux comprendre les dynamiques de réponse des biomarqueurs. Dans ce cadre, pour aborder cette problématique, une stratégie décomposée en deux sous-parties a été utilisée. Tout d’abord une étude de la partie « toxico-cinétique » ou TK a permis de relier la dose externe, présente dans l’environnement, à la dose interne, présente dans l’organisme. Puis, la partie « toxico-dynamique » ou TD a été développé pour faire le lien entre la dose interne et l’effet. Dans un premier temps, ce travail de thèse a consisté à collecter un ensemble de données TK et TD chez notre espèce-modèle, l’épinoche à trois épines, sur une famille de molécules, les bisphénols, et plus particulièrement, le BPA, le BPS et le BPF. Ces données récoltées à partir d’expositions de courte durée (sept jours de contamination et sept jours de dépuration) et d’une exposition de longue durée (21 jours) ont tout d’abord permis de comparer les effets de modulation des bisphénols sur les biomarqueurs. Les marqueurs de l’immunité innée ont notamment été fortement impactés par ces substances. Des différences de cinétique entre le BPA et le BPS ont par ailleurs été mise en avant. Par la suite, les données collectées au cours des expositions ont été utilisée pour construire un modèle TK à base physiologique (PBTK) pour le BPA, puis un modèle PBTK couplé à des sous-modèles TD (PBTK-TD) décrivant la dynamique de certains immunomarqueurs. Enfin, un dernier modèle PBTK-TD a été construit pour démontrer la faisabilité de cette démarche de modélisation pour intégrer des conditions d’exposition plus représentatives de celles du milieu naturel, i.e. pour un mélange de substances. Considéré dans son ensemble, ce travail de thèse démontre l’attractivité du couplage entre l’approche expérimentale par la mesure de biomarqueurs et la modélisation
Biomarkers are useful tools for the diagnosis of environmental risk in aquatic ecosystems. Nevertheless, the measurement of these sub-individual markers still presents some limitations for the assessment of ecosystem health, including the characterisation of the complex dynamics of responses of these non-lethal effects as a function of time or dose, or the extrapolation of responses from one scale of biological organisation to another. One of the solutions that seems promising for characterising the dynamics of these responses from a change of scale perspective would be to integrate the biomarkers into mechanistic models that make it possible to predict these dynamics and explain the mechanisms underlying the effects. This thesis proposes to build mechanistic models of physiologically based toxicokinetics and toxicodynamics (PBTK-TD) to better characterise and understand the response dynamics of biomarkers. In this context, the problem of biomarker dynamics was divided in two. First, the "toxico-kinetic" or TK makes it possible to link the external dose, present in the environment, to the internal dose, present in the organism. Second, the "toxico-dynamic" or TD, makes the link between the internal dose and the effect. Accordingly, the first step in this thesis was to collect a set of TK and TD data in our model species, the three-spined stickleback, on a family of compounds, the bisphenols, and more specifically, BPA, BPS and BPF. These data, collected from short-term exposures (seven days of contamination and seven days of depuration) and long-term exposure (21 days), were used to compare the modulating effects of bisphenols on biomarkers. In particular, markers of innate immunity were strongly impacted by these substances. Differences in kinetics between BPA and BPS were also highlighted. Subsequently, the data collected during the exposures were used to build a physiologically based TK model (PBTK) for BPA, then a PBTK model coupled with TD sub-models (PBTK-TD) describing the dynamics of certain immunomarkers in the stickleback. Finally, a last PBTK-TD model was built to demonstrate the feasibility of this modelling approach for integrating exposure conditions more representative of those in the natural environment, i.e. for a mixture of substances. Taken as a whole, this thesis demonstrates the attractiveness of coupling the experimental approach consisting in measuring biomarkers and modelling
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Chaumet, Betty. "Transfert et distribution des pesticides dans les biofilms en lien avec les effets toxiques associés." Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0223/document.

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En 2000, la Directive Cadre sur l’Eau a exigé le retour au bon état chimique et écologique des cours d’eau. Elle a notamment classé 45 substances comme étant prioritaires pour cette évaluation (directive 2013/39/UE), dont en grande partie des pesticides. En effet, en raison de leur utilisation massive, on retrouve aujourd’hui ces contaminants dans tous les compartiments de l’environnement. Par ailleurs, au vu de sa capacité à intégrer les contaminations, le biofilm est considéré comme un excellent bioindicateur pour l’évaluation de la qualité de l’eau. Celui-ci est à la base de la chaine trophique dans les milieux aquatiques et se compose de microorganismes (microalgues, bactéries, champignons, etc…) enchâssés dans une matrice de substances polymériques extracellulaires (EPS).Cette thèse porte sur l’étude des mécanismes de transfert et de distribution des pesticides dans les biofilms en lien avec les effets toxiques associés. Ces travaux ont été réalisés avec une approche toxicocinétique par laquelle la bioaccumulation du diuron (un herbicide inhibiteur de la photosynthèse) a été suivie dans les différents compartiments du biofilm. Ce suivi a été réalisé sous plusieurs conditions abiotiques (vitesses de courant, températures et photopériodes) pour différentes durées d’exposition. En parallèle des descripteurs fonctionnels et structuraux ont été mesurés comme des activités photosynthétique (pour les communautés autotrophes) et enzymatiques (pour les communautés hétérotrophes), ainsi que la biomasse totale, la production de protéines et de polysaccharides.L’ensemble des expérimentations menées au cours de cette thèse a permis de décrire les mécanismes de sorption du diuron dans les biofilms, à savoir des processus d’absorption par les cellules et d’adsorption par la matrice EPS. Puis l’influence des différents paramètres environnementaux étudiés a pu être mise en avant. Ces travaux démontrent la pertinence de l’approche toxicocinétique-toxicodynamique pour l’étude de l’impact des pesticides sur les biofilms fluviaux
In 2000, the Water Framework Directive required the return of rivers to good chemical and ecological status. In particular, it has classified 45 substances as priority for this assessment (Directive 2013/39/EU), including a large proportion of pesticides. Indeed, due to their massive use, these contaminants are now found in all compartments of the environment. In addition, given its ability to integrate contamination, biofilm is considered an excellent bioindicator for water quality assessment. It is at the base of the trophic chain in aquatic environments and is composed of microorganisms (microalgae, bacteria, fungi, etc...) embedded in a matrix of extracellular polymeric substances (EPS).This thesis focused on the analysis of mechanisms of pesticide transfer and distribution in biofilms related to toxic impacts. This work was carried out using a toxicokinetic approach whereby the bioaccumulation of diuron (a photosynthesis inhibitor herbicide) was monitored in the different compartments of the biofilm. This assessment was carried out under several abiotic conditions (flow velocity, temperatures and photoperiods) under varying exposure durations. In parallel, functional and structural descriptors were measured as photosynthetic (for autotrophic communities) and enzymatic (for heterotrophic communities) activities, as well as biofilm biomass and protein and polysaccharide production.All the experiments performed during this thesis made it possible to highlight the sorption mechanisms of diuron in biofilm, i.e. absorption processes by cells and adsorption phenomenon within the EPS matrix. Then the influence of the different environmental parameters studied was emphasized. This work demonstrates the relevance of the toxicokinetic-toxicodynamic approach to the study of the impact of pesticides on fluvial biofilms
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Lewandowski, Thomas A. "Toxicokinetic and toxicodynamic modeling of the effects of methyl mercury on development of the embryonic rat midbrain /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8450.

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Everett, Scott D. "The Pharmacodynamics and Toxicodynamics of Inotropic Drugs in Calves With Natural and Artificial Hearts." DigitalCommons@USU, 1994. https://digitalcommons.usu.edu/etd/4103.

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Inotropic support for the failing myocardium as the therapy for xi congestive heart failure (CHF) is intended to achieve an increase in cardiac output via positive responses in myocardial contractility and vasodilation. A novel approach to differentiate these two responses is the use of an animal with an implanted total artificial heart (TAH). Three inotropic drugs, dobutamine, enoximone, and pimobendan, were tested in eight animals with their natural heart intact and five animals implanted with a TAH. Baseline values of the TAH and natural heart (NH) were compared to determine their hemodynamic similarities. Each of the three drugs was given randomly to the animals in dosages similar to human clinical doses. Peak responses were recorded and analyzed. All three drugs caused an increase in contractility and cardiac output in the NH animals. Dobutamine and pimobendan also caused a significant increase in heart rate at higher dosages whereas enoximone did not. Dobutamine caused an increase in left ventricle work, as did pimobendan at the first dose given; at higher doses of pimobendan, the left ventricular work returned to baseline. However, at the doses tested, the left ventricular stroke work during enoximone administration decreased. Vasodilation (the only drug stimulation response in the TAH model) was also observed with the administration of the drugs in T AH animals, and all three caused decreases in systemic and pulmonary vascular resistance. Dobutamine and pimobendan caused an increase in left and right atrial pressures (because of the mechanical heart not being adjusted to compensate the increased return). There was also a reduction in systemic and pulmonary resistance. Enoximone caused severe pulmonary hypertension in the TAH animals, possibly due to stimulus of platelets to release vasoconstrictive substances. Thus, dobutamine, enoximone, and pimobendan significantly contribute to increases in output by vasodilation in animals with a natural heart. Similarly, dobutamine and pimobendan's vasodilatory action is identified in an animal with a TAH. However, enoximone's hypertensive action on the pulmonary vasculature of a TAH animal may offer an insight to the toxicity of enoximone when used after recent surgery.
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Berggren, Kristina. "Toxicity of chlorantraniliprole to the Collembola Folsomia candida : toxicodynamics and effects of organic matter content." Thesis, Mittuniversitetet, Avdelningen för naturvetenskap, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:miun:diva-24243.

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Toxicity of pesticides to non-target organisms determines their impact on natural environments. And to find pesticides with a new, target-specific mode of action, which are safe to farmers and organisms in the surrounding environment, is important when developing new pesticides.In this study, toxicity of the insecticide chlorantraniliprole to the Collembola Folsomia candida was investigated, showing that the test animals were adversely affected by the compound. Toxicity was tested in two experiments; a reproduction test in four soils with different organic matter content, following the OECD Guideline 232, and a toxicodynamic test where mortality, mobility, reproduction and morphological changes were recorded.The reproduction test showed a lower toxicity of chlorantraniliprole in the high-organic soils compared to the low-organic. When organic matter content increased two times, the difference between the lowest and the highest EC50 and EC10 values was a factor of 5.3 and 8.4, respectively. pH did not seem to significantly affect toxicity, and organic matter content did not seem to affect the total number of juveniles produced.The toxicodynamic test showed a fast mode of action on mobility of F. candida, but not on mortality. Mobility decreased at the highest treatments of chlorantraniliprole already one day after the animals were introduced to the test vessels, but significant mortality was still not seen after almost three weeks. Reproduction was also adversely affected with a decline in the total number of juveniles produced at the higher treatments. The animals at the higher treatments also showed a possible compound induced reproduction stress, with faster egg laying. Morphological changes, such as affected antennas, increased steadily over time.Chlorantraniliprole shows high toxicity to some non-target organisms but is, with its new mode of action, still important in the development of more environmentally safe pesticides.
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Heine, Simon [Verfasser]. "Development and specification of a toxicokinetic and toxicodynamic growth model of Myriophyllum spicatum for use in risk assessment / Simon Heine." Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2014. http://d-nb.info/1065353502/34.

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Dogruer, Gulsah. "Assessing the impact of chemical exposure on the health of endangered sea turtles through toxicokinetics and toxicodynamics." Thesis, Griffith University, 2022. http://hdl.handle.net/10072/420901.

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The green sea turtle, Chelonia mydas, spends a considerable part of its life in coastal waters foraging on seagrass and/or algae, which brings it close to anthropogenic pollutant sources. Elevated concentrations of chemical contaminants from urban, industrial and agricultural run-off accumulate in coastal environments. These pollutants have the potential to cause serious harm to C. mydas populations. However, exposure and toxicity data are challenging to obtain for free-ranging, protected wildlife species like C. mydas. Furthermore, a lack of quantitative tools linking long-term external contaminant exposure, the uptake and tissue distribution of chemicals (toxicokinetics), and the biological pathway perturbations related to adverse health outcomes (toxicodynamics) hamper efforts by scientists and policymakers to quantify the risk of pollutants adversely affecting C. mydas health. Changes in C. mydas population abundance, in turn, may affect the marine seagrass ecosystems, which, by extension, could potentially also impact human health and animals that rely on seagrass habitats. The present thesis provided the means to research the hypothesis that land-based contaminants adversely impact the health of Australia’s resident green turtle populations. The following chapters in this thesis investigate the validity of this hypothesis. Valuable experimental toxicokinetic and toxicodynamic data are collected and described in Chapters 2 and 3. Chapter 4 used data from Chapter 3 to develop tools to confirm the initial hypothesis. Overall, this thesis describes the development of tools to aid risk assessors and policymakers in setting safe chemical exposure levels for green sea populations.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Environment and Sc
Science, Environment, Engineering and Technology
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Collet, Séverine. "Développement d’une approche toxicocinétique/toxicodynamique basée sur des mécanismes physiologiques pour évaluer les effets oestrogéniques du Bisphénol A." Thesis, Toulouse, INPT, 2012. http://www.theses.fr/2012INPT0001/document.

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Ce travail a consisté à analyser, par des approches toxicocinétiques (TK) et mécanistiques, les effets oestrogéniques du Bisphenol A (BPA) sur un biomarqueur précoce et sensible : la sécrétion de l'hormone lutéinisante (LH) chez la brebis prépubère ovariectomisée. La plus faible concentration plasmatique en BPA induisant une inhibition de LH s'est avérée proche des concentrations maximales décrites chez l'Homme. Cette inhibition de LH pourrait impliquer une inhibition des systèmes neuronaux à kisspeptine. L'approche TK comparative d'espèces a montré que la clairance du BPA est toujours élevée, proche du débit sanguin hépatique. Pour une exposition à la dose journalière admissible, cette approche permet de prédire chez l'Homme des concentrations en BPA très inférieures à celles associées à une inhibition de LH dans notre modèle
The goal of this thesis was to analyse through toxicokinetic (TK) and mechanistic approaches the estrogeno-mimetic effects of bisphenol A (BPA) on a precocious and sensitive biomarker: LH secretion in ovariectomized female lambs. The lowest plasma BPA concentrations associated to an inhibition of LH secretion appeared to be close to the highest one reported in human. LH suppression could be mediated by an inhibition of hypothalamic kisspeptin systems. The multispecies TK approach showed that BPA clearance is always high and equivalent to the liver blood flow. For an exposure scheme corresponding to the tolerable daily intake, this approach allows to predict human BPA concentration much lower than the one associated to LH inhibition in our highly sensitive lamb model
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Black, Paleah. "Interactions of Dietary Antioxidants and Methylmercury on Health Outcomes and Toxicodynamics: Evidence from Developmental Rat Model Studies and Human Epidemiology." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19874.

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The contamination of seafood with methylmercury (MeHg) is a global health issue, as MeHg is a well known neurotoxin. Since dietary nutrients may interact with MeHg toxicity, and oxidative stress is one of the primary mechanisms underlying MeHg neurotoxicity, we characterized dietary antioxidant-MeHg interactions. Firstly, we used an ethnobotanical study to confirm the antioxidant activity of Northern Labrador Tea, Rhododendron tomentosum ssp. subarcticum (Tea), for the Canadian Inuit, a population with elevated MeHg exposure. Secondly, we determined the ability of Tea to ameliorate MeHg-induced toxicity in a rat perinatal exposure study. MeHg exposure (2 mg/KgBW/d) was associated with perturbed development and behaviour, elevated brain N-methyl-D-aspartate receptors, and serum lipid peroxidation. Surprisingly, Tea co-exposure (100 mg/KgBW/d) modulated MeHg’s effects on brain NMDA-R levels and lipid peroxidation, but also increased mercury serum concentrations. Thirdly, using a toxicogenomics approach we determined that MeHg exposure caused the down-regulation of Nr4a2 and its protein product Nurr1. These novel MeHg targets are implicated in developmental learning functions and were corrected with MeHg + Tea co-exposure. Lastly, we conducted a risk assessment survey and cross-sectional dietary epidemiology study in Costa Rica to further investigate dietary nutrient-MeHg interactions. Costa Rica is a Central American country with multiple sources of Hg and a high per capital fish consumption. Here, 5 of the 14 populations we studied exceeded the recommended MeHg provisional tolerable daily intake (pTDI) of 0.2 µg/KgBW/d. In Heredia the pTDI was exceeded by 34% of woman participants, primarily associated with canned tuna consumption. Interestingly, we detected that Hg body burden was significantly reduced by the consumption of antioxidant-rich dietary items. Considering our collective results, we hypothesized that MeHg toxicokinetics may be altered by dietary nutrients at the site of intestinal absorption from the disruption of gut flora, or at the site of cellular demethylation in tissues from the improvement of cellular redox state. The interaction of dietary nutrients on MeHg outcomes has a large impact on risk assessment and may provide a public health approach for managing the risk associated with MeHg exposure without reducing local fish consumption.
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Gajewska, Monika Anna [Verfasser], Karl-Werner [Akademischer Betreuer] [Gutachter] Schramm, and Heiko [Gutachter] Briesen. "Physiologically-based toxicokinetic and toxicodynamic modelling of single and repeated dose toxicity / Monika Anna Gajewska. Betreuer: Karl-Werner Schramm. Gutachter: Karl-Werner Schramm ; Heiko Briesen." München : Universitätsbibliothek der TU München, 2015. http://d-nb.info/1101695188/34.

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Books on the topic "Toxicodynamie"

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Tou, Grace. The pharmacokinetics of 2-acetamido-P-cresol and the effects of deacetylation on its toxicodynamics. Ottawa: National Library of Canada, 1991.

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Drug Toxicodynamics (Drugs and the Pharmaceutical Sciences). Marcel Dekker Inc, 2006.

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Tekade, Rakesh Kumar. Essentials of Pharmatoxicology in Drug Research, Volume 1: Toxicity and Toxicodynamics. Elsevier Science & Technology Books, 2023.

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Essentials of Pharmatoxicology in Drug Research, Volume 1: Toxicity and Toxicodynamics. Elsevier Science & Technology, 2023.

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Tekade, Rakesh Kumar. Public Health and Toxicology Issues in Drug Research, Volume 2: Toxicity and Toxicodynamics. Elsevier Science & Technology Books, 2023.

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Tou, Grace. The pharmacokinetics of 2-acetamido-P-cresol and the effects of deacetylation on its toxicodynamics. 1991.

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Book chapters on the topic "Toxicodynamie"

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Cartus, Alexander, and Dieter Schrenk. "Toxicodynamic Tests." In Regulatory Toxicology, 1–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/978-3-642-36206-4_39-2.

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Edler, Lutz. "Toxicodynamic Models." In Regulatory Toxicology, 1–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/978-3-642-36206-4_48-2.

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Philip, Binu K., S. Satheesh Anand, and Harihara M. Mehendale. "Toxicodynamic Interactions." In Principles and Practice of Mixtures Toxicology, 159–206. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2010. http://dx.doi.org/10.1002/9783527630196.ch6.

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Schrenk, Dieter. "Toxicodynamic Tests." In Regulatory Toxicology, 161–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-35374-1_39.

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Edler, Lutz, and Angelika Tritscher. "Toxicodynamic Models." In Regulatory Toxicology, 261–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-35374-1_48.

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Edler, Lutz. "Toxicodynamic Models." In Regulatory Toxicology, 397–405. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57499-4_48.

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Cartus, Alexander, and Dieter Schrenk. "Toxicodynamic Tests." In Regulatory Toxicology, 215–29. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57499-4_39.

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Herber, Robert F. M. "Toxicokinetics and toxicodynamics - 1." In Fundamental Toxicology for Chemists, 17–25. Cambridge: Royal Society of Chemistry, 2007. http://dx.doi.org/10.1039/9781847550941-00017.

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Renwick, Andrew G. "Toxicokinetics and toxicodynamics - 2." In Fundamental Toxicology for Chemists, 26–42. Cambridge: Royal Society of Chemistry, 2007. http://dx.doi.org/10.1039/9781847550941-00026.

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Burcham, Philip C. "Toxicodynamics: How Chemicals Harm Cells." In An Introduction to Toxicology, 91–125. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-5553-9_4.

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Conference papers on the topic "Toxicodynamie"

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Wittemer-Rump, Sabine, Anette Sommer, Charlotte Kopitz, Hung Huynh, Christoph Schatz, Ruprecht Zierz, Manuela Braun, et al. "Abstract 1683: Pharmacokinetic/pharmacodynamic (PK/PD) and toxicokinetic/toxicodynamic (TK/TD) modeling of preclinical data of FGFR2-ADC (BAY 1187982) to guide dosing in phase 1." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1683.

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