AOP report: Development of an adverse outcome pathway for oxidative DNA damage leading to mutations and chromosomal aberrations

The Genetic Toxicology Technical Committee (GTTC) of the Health and Environmental Sciences Institute (HESI) is developing adverse outcome pathways (AOPs) that describe modes of action leading to potentially heritable genomic damage. The goal was to enhance the use of mechanistic information in genot...

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Published inEnvironmental and molecular mutagenesis Vol. 63; no. 3; pp. 118 - 134
Main Authors Cho, Eunnara, Allemang, Ashley, Audebert, Marc, Chauhan, Vinita, Dertinger, Stephen, Hendriks, Giel, Luijten, Mirjam, Marchetti, Francesco, Minocherhomji, Sheroy, Pfuhler, Stefan, Roberts, Daniel J., Trenz, Kristina, Yauk, Carole L.
Format Journal Article
LanguageEnglish
Published Hoboken, USA John Wiley & Sons, Inc 01.03.2022
Wiley Subscription Services, Inc
Wiley-Blackwell
Subjects
Antioxidants
Aop Report
Chromosome aberrations
Damage
Deoxyribonucleic acid
DNA
DNA damage
DNA repair
Environmental science
Free radicals
Genotoxicity
Intermediates
Life Sciences
Mutation
Reactive oxygen species
Repair
Toxicology
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Abstract The Genetic Toxicology Technical Committee (GTTC) of the Health and Environmental Sciences Institute (HESI) is developing adverse outcome pathways (AOPs) that describe modes of action leading to potentially heritable genomic damage. The goal was to enhance the use of mechanistic information in genotoxicity assessment by building empirical support for the relationships between relevant molecular initiating events (MIEs) and regulatory endpoints in genetic toxicology. Herein, we present an AOP network that links oxidative DNA damage to two adverse outcomes (AOs): mutations and chromosomal aberrations. We collected empirical evidence from the literature to evaluate the key event relationships between the MIE and the AOs, and assessed the weight of evidence using the modified Bradford‐Hill criteria for causality. Oxidative DNA damage is constantly induced and repaired in cells given the ubiquitous presence of reactive oxygen species and free radicals. However, xenobiotic exposures may increase damage above baseline levels through a variety of mechanisms and overwhelm DNA repair and endogenous antioxidant capacity. Unrepaired oxidative DNA base damage can lead to base substitutions during replication and, along with repair intermediates, can also cause DNA strand breaks that can lead to mutations and chromosomal aberrations if not repaired adequately. This AOP network identifies knowledge gaps that could be filled by targeted studies designed to better define the quantitative relationships between key events, which could be leveraged for quantitative chemical safety assessment. We anticipate that this AOP network will provide the building blocks for additional genotoxicity‐associated AOPs and aid in designing novel integrated testing approaches for genotoxicity.
AbstractList he Genetic Toxicology Technical Committee (GTTC) of the Health and Environmental Sciences Institute (HESI) is developing adverse outcome pathways (AOPs) that describe modes of action leading to potentially heritable genomic damage. The goal is to enhance the use of mechanistic information in genotoxicity assessment by building empirical support for the relationships between relevant molecular initiating events (MIEs) and regulatory endpoints in genetic toxicology. Herein, we present an AOP network that links oxidative DNA damage to two adverse outcomes (AOs): mutations and chromosomal aberrations. We collected empirical evidence from the literature to evaluate the key event relationships between the MIE and the AOs, and assessed the weight of evidence using the modified Bradford-Hill criteria for causality. Oxidative DNA damage is constantly induced and repaired in cells given the ubiquitous presence of reactive oxygen species and free radicals. However, xenobiotic exposures may increase damage above baseline levels through a variety of mechanisms and overwhelm DNA repair and endogenous antioxidant capacity. Unrepaired oxidative DNA base damage can lead to base substitutions during replication and, along with repair intermediates, can also cause DNA strand breaks that can lead to mutations and chromosomal aberrations if not repaired adequately. This AOP network identifies knowledge gaps that could be filled by targeted studies designed to better define the quantitative relationships between key events, which could be leveraged for quantitative chemical safety assessment. We anticipate that this AOP network will provide the building blocks for additional genotoxicity-associated AOPs and aid in designing novel integrated testing approaches for genotoxicity.
The Genetic Toxicology Technical Committee (GTTC) of the Health and Environmental Sciences Institute (HESI) is developing adverse outcome pathways (AOPs) that describe modes of action leading to potentially heritable genomic damage. The goal was to enhance the use of mechanistic information in genotoxicity assessment by building empirical support for the relationships between relevant molecular initiating events (MIEs) and regulatory endpoints in genetic toxicology. Herein, we present an AOP network that links oxidative DNA damage to two adverse outcomes (AOs): mutations and chromosomal aberrations. We collected empirical evidence from the literature to evaluate the key event relationships between the MIE and the AOs, and assessed the weight of evidence using the modified Bradford-Hill criteria for causality. Oxidative DNA damage is constantly induced and repaired in cells given the ubiquitous presence of reactive oxygen species and free radicals. However, xenobiotic exposures may increase damage above baseline levels through a variety of mechanisms and overwhelm DNA repair and endogenous antioxidant capacity. Unrepaired oxidative DNA base damage can lead to base substitutions during replication and, along with repair intermediates, can also cause DNA strand breaks that can lead to mutations and chromosomal aberrations if not repaired adequately. This AOP network identifies knowledge gaps that could be filled by targeted studies designed to better define the quantitative relationships between key events, which could be leveraged for quantitative chemical safety assessment. We anticipate that this AOP network will provide the building blocks for additional genotoxicity-associated AOPs and aid in designing novel integrated testing approaches for genotoxicity.The Genetic Toxicology Technical Committee (GTTC) of the Health and Environmental Sciences Institute (HESI) is developing adverse outcome pathways (AOPs) that describe modes of action leading to potentially heritable genomic damage. The goal was to enhance the use of mechanistic information in genotoxicity assessment by building empirical support for the relationships between relevant molecular initiating events (MIEs) and regulatory endpoints in genetic toxicology. Herein, we present an AOP network that links oxidative DNA damage to two adverse outcomes (AOs): mutations and chromosomal aberrations. We collected empirical evidence from the literature to evaluate the key event relationships between the MIE and the AOs, and assessed the weight of evidence using the modified Bradford-Hill criteria for causality. Oxidative DNA damage is constantly induced and repaired in cells given the ubiquitous presence of reactive oxygen species and free radicals. However, xenobiotic exposures may increase damage above baseline levels through a variety of mechanisms and overwhelm DNA repair and endogenous antioxidant capacity. Unrepaired oxidative DNA base damage can lead to base substitutions during replication and, along with repair intermediates, can also cause DNA strand breaks that can lead to mutations and chromosomal aberrations if not repaired adequately. This AOP network identifies knowledge gaps that could be filled by targeted studies designed to better define the quantitative relationships between key events, which could be leveraged for quantitative chemical safety assessment. We anticipate that this AOP network will provide the building blocks for additional genotoxicity-associated AOPs and aid in designing novel integrated testing approaches for genotoxicity.
The Genetic Toxicology Technical Committee (GTTC) of the Health and Environmental Sciences Institute (HESI) is developing adverse outcome pathways (AOPs) that describe modes of action leading to potentially heritable genomic damage. The goal was to enhance the use of mechanistic information in genotoxicity assessment by building empirical support for the relationships between relevant molecular initiating events (MIEs) and regulatory endpoints in genetic toxicology. Herein, we present an AOP network that links oxidative DNA damage to two adverse outcomes (AOs): mutations and chromosomal aberrations. We collected empirical evidence from the literature to evaluate the key event relationships between the MIE and the AOs, and assessed the weight of evidence using the modified Bradford-Hill criteria for causality. Oxidative DNA damage is constantly induced and repaired in cells given the ubiquitous presence of reactive oxygen species and free radicals. However, xenobiotic exposures may increase damage above baseline levels through a variety of mechanisms and overwhelm DNA repair and endogenous antioxidant capacity. Unrepaired oxidative DNA base damage can lead to base substitutions during replication and, along with repair intermediates, can also cause DNA strand breaks that can lead to mutations and chromosomal aberrations if not repaired adequately. This AOP network identifies knowledge gaps that could be filled by targeted studies designed to better define the quantitative relationships between key events, which could be leveraged for quantitative chemical safety assessment. We anticipate that this AOP network will provide the building blocks for additional genotoxicity-associated AOPs and aid in designing novel integrated testing approaches for genotoxicity.
Author Allemang, Ashley
Yauk, Carole L.
Hendriks, Giel
Pfuhler, Stefan
Trenz, Kristina
Luijten, Mirjam
Audebert, Marc
Roberts, Daniel J.
Chauhan, Vinita
Dertinger, Stephen
Minocherhomji, Sheroy
Marchetti, Francesco
Cho, Eunnara
AuthorAffiliation 6 Litron Laboratories Rochester New York USA
11 Ingelheim Pharma GmbH & Co.KG Biberach Germany
2 Department of Biology Carleton University Ottawa Ontario Canada
9 Amgen Research, Translational Safety and Bioanalytical Sciences Amgen Inc. Thousand Oaks California USA
10 Charles River Laboratories Skokie Illinois USA
5 Consumer and Clinical Radiation Protection Bureau Health Canada Ottawa Ontario Canada
4 Toxalim, UMR1331 INRAE Toulouse France
8 Centre for Health Protection National Institute for Public Health and the Environment (RIVM) Bilthoven The Netherlands
12 Department of Biology University of Ottawa Ottawa Ontario Canada
1 Environmental Health Science and Research Bureau Health Canada Ottawa Ontario Canada
3 The Procter & Gamble Company Mason Ohio USA
7 Toxys Leiden The Netherlands
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  orcidid: 0000-0002-6725-3454
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  organization: University of Ottawa
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35315142$$D View this record in MEDLINE/PubMed
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2022 The Authors. Environmental and Molecular Mutagenesis published by Wiley Periodicals LLC on behalf of Environmental Mutagen Society.
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Natural Science and Engineering Council of Canada (NSERC)’s Collaborative Research and Training (CREATE) Program; Health Canada's Genomics Research and Development Initiative
J. OBrien
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Funding information Natural Science and Engineering Council of Canada (NSERC)’s Collaborative Research and Training (CREATE) Program; Health Canada's Genomics Research and Development Initiative
Accepted by: J. OBrien
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PublicationTitle Environmental and molecular mutagenesis
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Snippet The Genetic Toxicology Technical Committee (GTTC) of the Health and Environmental Sciences Institute (HESI) is developing adverse outcome pathways (AOPs) that...
he Genetic Toxicology Technical Committee (GTTC) of the Health and Environmental Sciences Institute (HESI) is developing adverse outcome pathways (AOPs) that...
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SubjectTerms Antioxidants
Aop Report
Chromosome aberrations
Damage
Deoxyribonucleic acid
DNA
DNA damage
DNA repair
Environmental science
Free radicals
Genotoxicity
Intermediates
Life Sciences
Mutation
Reactive oxygen species
Repair
Toxicology
Title AOP report: Development of an adverse outcome pathway for oxidative DNA damage leading to mutations and chromosomal aberrations
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fem.22479
https://www.ncbi.nlm.nih.gov/pubmed/35315142
https://www.proquest.com/docview/2662537871
https://www.proquest.com/docview/2641864765
https://hal.inrae.fr/hal-03624340
https://pubmed.ncbi.nlm.nih.gov/PMC9322445
Volume 63
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