Pseudocholinesterase polymorphism in an Irish population

Adebayo, Gani I.; Williams, John W; Healy, Selena

doi:10.1016/j.ejim.2005.03.004

Cited by 3 publications

(1 citation statement)

References 19 publications

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“…However, no inter-individual variability was available from this review and the authors concluded that the OP insecticide levels measured in the epidemiologic studies are too low to cause biologically meaningful acetylcholinesterase inhibition, the most widely used metric for OP insecticide toxicity. At the end, 13 studies were included in the Excel database (Adebayo et al, 2005;Farahat et al, 2011;Garabrant et al, 2009;Gordon et al, 2005;Keegan et al, 2017;Lefevre et al, 2009;Mak et al, 2014;Marino et al, 1998;Ohayo-Mitoko et al, 2000;Poet et al, 2017b;Seng et al, 2009;Vaisi-Raygani et al, 2007;Wafa et al, 2013). Collected parameters related to inter-individual variability in Cholinesterase inhibition were harmonized and converted into coefficient of variation (CV) in order to be comparable to each other.…”

Section: Pharmacodynamics (Pd)/toxicodynamics (Td) For Neurotoxic Acetylcholine Esterase (Ache) Inhibitorsmentioning

confidence: 99%

Modelling human variability in toxicokinetic and toxicodynamic processes using Bayesian meta‐analysis, physiologically‐based modelling and in vitro systems

Testai

Béchaux

Buratti

et al. 2021

EFSA Supporting Publications

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This external scientific report summarises the results from the article 36 grant GA/EFSA/SCER/2015/01 "Modelling human variability in toxicokinetic and toxicodynamic processes using Bayesian meta-analysis, physiologically-based (PB) modelling and in vitro systems". Extensive literature searches, data collection and modelling of human variability in toxicokinetics (TK) (phase I, Phase II enzymes and transporters) and toxicodynamics (TD) are summarised and further elaborated in supplementary material and EFSA knowledge junction, open source databases (MS Excel) and peer reviewed publications (objective 1 and 2). In addition, in vitro TK and TD information from laboratory studies and literature searches are summarised for a range of case studies relevant to EFSA including pesticides (i.e. triflumuron, chlorpyrifos, phosmet), natural toxins (e.g. microcystin variants, mycotoxins), food additives and polyphenols (i.e. resveratrol, tyrosol), food additives as well as drugs (i.e. amiodarone). These include isoform-specific metabolism and kinetic parameters for single chemicals and inhibition constants for multiple chemicals (TK) and identification of molecular targets (TD). Finally, generic quantitative in vitro in vivo extrapolation (QIVIVE) models, PB-kinetic (PBK) and PBK-dynamic (PBKD) models were developed in the R freeware, calibrated and validated using case studies for single and multiple chemicals. Supplementary material and model codes are available on EFSA knowledge junction. The results are in line with EFSA priorities for the implementation of the use of new approach methodologies (NAMs) for human risk assessment (RA) of chemicals and the need to develop open source TK TD databases data and PB-K and PB-KD models have been identified as key steps of this process. Future perspectives are discussed including the integration of pathway-related variability and generic human QIVIVE and PB-K models and PB-K-D models into TKplate, a Toxicokinetic Modelling Platform under development in EFSA.

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