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.

Bibliographic Details
Main Authors: 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
Format: Article
Language:English
Published: Nature Portfolio 2022-02-01
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.
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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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