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  • 27-April-2023

    English

    Children’s Health

    Children can be more vulnerable to environmental hazards posed by chemicals, due to their physiological differences and unique behaviour. This document presents the results of a survey conducted in 2021, aiming to identify currently available methodologies for assessing the risk of chemicals to children’s health and also identify possible needs for additional or missing parameters and for further guidance documents.

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  • 13-April-2023

    English

    eChemPortal: Global Portal to Information on Chemical Substances

    This Guidance provides concise and practical information to help organisations identify the type of chemicals information shared on the eChemPortal - the Global Portal to Information on Chemical Substances and to define the best strategy to participate as a data source.

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  • 15-March-2023

    English

    Safety of novel foods and feeds and on the harmonisation of regulatory oversight in biotechnology

    These two documents compile information on activities related to the assessment of the safety of products derived from modern biotechnology, environmental safety (biosafety) and the safety of novel foods and feeds, at the international level between April 2021 and May 2022. The information was provided by OECD Members, partner countries and observer organisations participating in the work.

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  • 15-December-2022

    English

    Deiodinase 2 inhibition leading to increased mortality via reduced posterior swim bladder inflation

    This Adverse Outcome Pathway (AOP) describes the linkage between Deiodinase 2 inhibition and increased mortality via reduced posterior swim bladder inflation. The swim bladder is a gas-filled organ found in many bony fish species and typically consists of two gas-filled chambers. The posterior chamber inflates during early development (embryo), while the anterior chamber inflates during late development (larva). Both chambers are important for fish to control buoyancy and the anterior chamber has an additional role in hearing. This AOP is part of a network of 5 AOPs describing how disruption of the thyroid hormone system can affect developmental processes involved in swim bladder inflation. The network includes three molecular initiating events representing the inhibition of enzymes that are important for thyroid hormone synthesis and activation. It describes how inhibition of thyroperoxidase and/or deiodinase, leads to reduced swim bladder inflation, resulting in reduced swimming performance, increased mortality and ultimately, decreased population trajectory in fish. This AOP network is currently mainly based on experimental evidence from studies on fish species with a two-chambered swim bladder. This AOP is referred to as AOP 155 in the Collaborative Adverse Outcome Pathway Wiki (AOP-Wiki).

  • 15-December-2022

    English

    Inhibitor binding to topoisomerase II leading to infant leukaemia

    This Adverse Outcome Pathway (AOP) describes the linkages between the perturbation of the normal topoisomerase II enzyme function and infant leukaemia. Infant leukaemia is a rare haematological disease (1 in 106 newborns, accounting for 10% of all childhood acute lymphoblastic leukaemias) of developmental origin, manifesting soon after birth (< 1 year old). The present AOP describes how interference of stressors with DNA topoisomerase II enzyme can possibly result in DNA double-strand break and chromosomal rearrangement during intrauterine development and lead to infant leukaemia, manifesting soon after birth. The proposed AOP is supported by a number of evidences by means of using etoposide as a model compound to empirically support the linkage between the proposed molecular initiating event and the adverse outcome. This AOP also identifies several knowledge gaps, the main ones being the identification of the initiating cell and the investigation of TopoII poisons in a robust model; thus, the present AOP may be modified in future on the basis of new evidence. This AOP is referred to as AOP 202 in the Collaborative Adverse Outcome Pathway Wiki (AOP-Wiki).

  • 15-December-2022

    English

    Deiodinase 1 inhibition leading to increased mortality via reduced posterior swim bladder inflation

    This Adverse Outcome Pathway (AOP) describes the linkage between Deiodinase 1 inhibition and increased mortality via reduced posterior swim bladder inflation. The swim bladder is a gas-filled organ found in many bony fish species and typically consists of two gas-filled chambers. The posterior chamber inflates during early development (embryo), while the anterior chamber inflates during late development (larva). Both chambers are important for fish to control buoyancy and the anterior chamber has an additional role in hearing. This AOP is part of a network of 5 AOPs describing how disruption of the thyroid hormone system can affect developmental processes involved in swim bladder inflation. The network includes three molecular initiating events representing the inhibition of enzymes that are important for thyroid hormone synthesis and activation. It describes how inhibition of thyroperoxidase and/or deiodinase, leads to reduced swim bladder inflation, resulting in reduced swimming performance, increased mortality and ultimately, decreased population trajectory in fish. This AOP network is currently mainly based on experimental evidence from studies on fish species with a two-chambered swim bladder. This AOP is referred to as AOP 157 in the Collaborative Adverse Outcome Pathway Wiki (AOP-Wiki).

  • 15-December-2022

    English

    Deiodinase 2 inhibition leading to increased mortality via reduced anterior swim bladder inflation

    This Adverse Outcome Pathway (AOP) describes the linkage between Deiodinase 2 inhibition and increased mortality via reduced anterior swim bladder inflation. The swim bladder is a gas-filled organ found in many bony fish species and typically consists of two gas-filled chambers. The posterior chamber inflates during early development (embryo), while the anterior chamber inflates during late development (larva). Both chambers are important for fish to control buoyancy and the anterior chamber has an additional role in hearing. This AOP is part of a network of 5 AOPs describing how disruption of the thyroid hormone system can affect developmental processes involved in swim bladder inflation. The network includes three molecular initiating events representing the inhibition of enzymes that are important for thyroid hormone synthesis and activation. It describes how inhibition of thyroperoxidase and/or deiodinase, leads to reduced swim bladder inflation, resulting in reduced swimming performance, increased mortality and ultimately, decreased population trajectory in fish. This AOP network is currently mainly based on experimental evidence from studies on fish species with a two-chambered swim bladder. This AOP is referred to as AOP 156 in the Collaborative Adverse Outcome Pathway Wiki (AOP-Wiki).

  • 15-December-2022

    English

    Deiodinase 1 inhibition leading to increased mortality via reduced anterior swim bladder inflation

    This Adverse Outcome Pathway (AOP) describes the linkage between Deiodinase 1 inhibition and increased mortality via reduced anterior swim bladder inflation. The swim bladder is a gas-filled organ found in many bony fish species and typically consists of two gas-filled chambers. The posterior chamber inflates during early development (embryo), while the anterior chamber inflates during late development (larva). Both chambers are important for fish to control buoyancy and the anterior chamber has an additional role in hearing. This AOP is part of a network of 5 AOPs describing how disruption of the thyroid hormone system can affect developmental processes involved in swim bladder inflation. The network includes three molecular initiating events representing the inhibition of enzymes that are important for thyroid hormone synthesis and activation. It describes how inhibition of thyroperoxidase and/or deiodinase, leads to reduced swim bladder inflation, resulting in reduced swimming performance, increased mortality and ultimately, decreased population trajectory in fish. This AOP network is currently mainly based on experimental evidence from studies on fish species with a two-chambered swim bladder. This AOP is referred to as AOP 158 in the Collaborative Adverse Outcome Pathway Wiki (AOP-Wiki).

  • 15-December-2022

    English

    Binding of electrophilic chemicals to SH(thiol)-group of proteins and /or to seleno-proteins involved in protection against oxidative stress during brain development leading to impairment of learning and memory

    This Adverse Outcome Pathway (AOP) describes the linkage between binding to proteins involved in protection against oxidative stress and impairment in learning and memory. Production, binding and degradation of Reactive Oxygen Radicals are tightly regulated in the body, and an imbalance between production and protection may cause oxidative stress, which is common to many toxicity pathways. Oxidative stress may lead to an imbalance in glutamate neurotransmission, which is involved in learning and memory. Oxidative stress may also cause cellular injury and death. During brain development and in particular during the establishment of neuronal connections and networks, such perturbations may lead to functional impairment in learning and memory. The weight-of-evidence supporting the relationship between the key events described in this AOP is based mainly on developmental effects observed after an exposure to mercury, a heavy metal known for its strong affinity to many proteins having anti-oxidant properties. This AOP is referred to as AOP 17 in the Collaborative Adverse Outcome Pathway Wiki (AOP-Wiki).

  • 15-December-2022

    English

    Uncoupling of oxidative phosphorylation leading to growth inhibition via decreased cell proliferation

    This Adverse Outcome Pathway (AOP) describes the linkage between uncoupling of oxidative phosphorylation (OXPHOS) and growth inhibition via decreased cell proliferation. The mitochondrial OXPHOS machinery is a key physiological process responsible for producing the primary cellular energy, adenosine triphosphate (ATP). Uncoupling of OXPHOS is a well-known mechanism of action of many chemicals and can affect many ATP-dependent biological functions. Cell proliferation in particular, as a major process to achieve organismal growth, is positively correlated with the cellular ATP level and highly susceptible to energy depletion. This AOP causally links uncoupling of OXPHOS to growth inhibition, through ATP depletion and reduced cell proliferation with strong weight of evidence support. This AOP is of high regulatory relevance, as it is considered applicable to both human health and ecological risk assessments. The AOP also forms the core of a larger AOP network addressing uncoupling of OXPHOS mediated growth inhibition. This AOP is referred to as AOP 263 in the Collaborative Adverse Outcome Pathway Wiki (AOP-Wiki).
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