Endogenous formaldehyde scavenges cellular glutathione resulting in redox disruption and cytotoxicity
Formaldehyde (FA) is known to exert cytotoxicity through DNA damage. Here, the authors show that FA also triggers cellular redox imbalance by reacting with glutathione (GSH), and that FA cytotoxicity is prevented by GSH synthesis and by ADH5, an enzyme that metabolizes FA-GSH products.
Main Authors: | , , , , , , , , , , , , , , |
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Format: | Article |
Language: | English |
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Nature Portfolio
2022-02-01
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Series: | Nature Communications |
Online Access: | https://doi.org/10.1038/s41467-022-28242-7 |
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author | Carla Umansky Agustín E. Morellato Matthias Rieckher Marco A. Scheidegger Manuela R. Martinefski Gabriela A. Fernández Oleg Pak Ksenia Kolesnikova Hernán Reingruber Mariela Bollini Gerry P. Crossan Natascha Sommer María Eugenia Monge Björn Schumacher Lucas B. Pontel |
author_facet | Carla Umansky Agustín E. Morellato Matthias Rieckher Marco A. Scheidegger Manuela R. Martinefski Gabriela A. Fernández Oleg Pak Ksenia Kolesnikova Hernán Reingruber Mariela Bollini Gerry P. Crossan Natascha Sommer María Eugenia Monge Björn Schumacher Lucas B. Pontel |
author_sort | Carla Umansky |
collection | DOAJ |
description | Formaldehyde (FA) is known to exert cytotoxicity through DNA damage. Here, the authors show that FA also triggers cellular redox imbalance by reacting with glutathione (GSH), and that FA cytotoxicity is prevented by GSH synthesis and by ADH5, an enzyme that metabolizes FA-GSH products. |
first_indexed | 2024-12-20T16:22:24Z |
format | Article |
id | doaj.art-653aae910d4d4b0192f151bf36477da9 |
institution | Directory Open Access Journal |
issn | 2041-1723 |
language | English |
last_indexed | 2024-12-20T16:22:24Z |
publishDate | 2022-02-01 |
publisher | Nature Portfolio |
record_format | Article |
series | Nature Communications |
spelling | doaj.art-653aae910d4d4b0192f151bf36477da92022-12-21T19:33:34ZengNature PortfolioNature Communications2041-17232022-02-0113111510.1038/s41467-022-28242-7Endogenous formaldehyde scavenges cellular glutathione resulting in redox disruption and cytotoxicityCarla Umansky0Agustín E. Morellato1Matthias Rieckher2Marco A. Scheidegger3Manuela R. Martinefski4Gabriela A. Fernández5Oleg Pak6Ksenia Kolesnikova7Hernán Reingruber8Mariela Bollini9Gerry P. Crossan10Natascha Sommer11María Eugenia Monge12Björn Schumacher13Lucas B. Pontel14Instituto de Investigación en Biomedicina de Buenos Aires (IBioBA), CONICET - Partner Institute of the Max Planck SocietyInstituto de Investigación en Biomedicina de Buenos Aires (IBioBA), CONICET - Partner Institute of the Max Planck SocietyInstitute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne, and Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), and Center for Molecular Medicine Cologne (CMMC)Instituto de Investigación en Biomedicina de Buenos Aires (IBioBA), CONICET - Partner Institute of the Max Planck SocietyCentro de Investigaciones en Bionanociencias (CIBION), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET)Centro de Investigaciones en Bionanociencias (CIBION), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET)Justus-Liebig University, Excellence Cluster Cardio-Pulmonary Institute (CPI), Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Center for Lung Research (DZL)Institute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne, and Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), and Center for Molecular Medicine Cologne (CMMC)Instituto de Investigación en Biomedicina de Buenos Aires (IBioBA), CONICET - Partner Institute of the Max Planck SocietyCentro de Investigaciones en Bionanociencias (CIBION), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET)MRC Laboratory of Molecular Biology, Cambridge Biomedical Campus, Francis Crick AvenueJustus-Liebig University, Excellence Cluster Cardio-Pulmonary Institute (CPI), Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Center for Lung Research (DZL)Centro de Investigaciones en Bionanociencias (CIBION), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET)Institute for Genome Stability in Ageing and Disease, Medical Faculty, University of Cologne, and Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD), and Center for Molecular Medicine Cologne (CMMC)Instituto de Investigación en Biomedicina de Buenos Aires (IBioBA), CONICET - Partner Institute of the Max Planck SocietyFormaldehyde (FA) is known to exert cytotoxicity through DNA damage. Here, the authors show that FA also triggers cellular redox imbalance by reacting with glutathione (GSH), and that FA cytotoxicity is prevented by GSH synthesis and by ADH5, an enzyme that metabolizes FA-GSH products.https://doi.org/10.1038/s41467-022-28242-7 |
spellingShingle | Carla Umansky Agustín E. Morellato Matthias Rieckher Marco A. Scheidegger Manuela R. Martinefski Gabriela A. Fernández Oleg Pak Ksenia Kolesnikova Hernán Reingruber Mariela Bollini Gerry P. Crossan Natascha Sommer María Eugenia Monge Björn Schumacher Lucas B. Pontel Endogenous formaldehyde scavenges cellular glutathione resulting in redox disruption and cytotoxicity Nature Communications |
title | Endogenous formaldehyde scavenges cellular glutathione resulting in redox disruption and cytotoxicity |
title_full | Endogenous formaldehyde scavenges cellular glutathione resulting in redox disruption and cytotoxicity |
title_fullStr | Endogenous formaldehyde scavenges cellular glutathione resulting in redox disruption and cytotoxicity |
title_full_unstemmed | Endogenous formaldehyde scavenges cellular glutathione resulting in redox disruption and cytotoxicity |
title_short | Endogenous formaldehyde scavenges cellular glutathione resulting in redox disruption and cytotoxicity |
title_sort | endogenous formaldehyde scavenges cellular glutathione resulting in redox disruption and cytotoxicity |
url | https://doi.org/10.1038/s41467-022-28242-7 |
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