<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Viau M</submitter><funding>Institut National Du Cancer</funding><funding>Agence Nationale de la Recherche</funding><funding>Commissariat Général à l&amp;apos;Investissement</funding><funding>Cancéropôle CLARA</funding><pagination>1462</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8533583</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(10)</volume><pubmed_abstract>Despite a considerable amount of data, the molecular and cellular bases of the toxicity due to metal exposure remain unknown. Recent mechanistic models from radiobiology have emerged, pointing out that the radiation-induced nucleo-shuttling of the ATM protein (RIANS) initiates the recognition and the repair of DNA double-strand breaks (DSB) and the final response to genotoxic stress. In order to document the role of ATM-dependent DSB repair and signalling after metal exposure, we applied twelve different metal species representing nine elements (Al, Cu, Zn Ni, Pd, Cd, Pb, Cr, and Fe) to human skin, mammary, and brain cells. Our findings suggest that metals may directly or indirectly induce DSB at a rate that depends on the metal properties and concentration, and tissue type. At specific me</pubmed_abstract><journal>Biomolecules</journal><pubmed_title>DNA Double-Strand Breaks Induced in Human Cells by Twelve Metallic Species: Quantitative Inter-Comparisons and Influence of the ATM Protein.</pubmed_title><pmcid>PMC8533583</pmcid><funding_grant_id>INDIRA Project</funding_grant_id><funding_grant_id>EURIPIDE Project</funding_grant_id><funding_grant_id>PROUST Project</funding_grant_id><funding_grant_id>HEMI-BREAKS Project</funding_grant_id><pubmed_authors>Fervers B</pubmed_authors><pubmed_authors>Viau M</pubmed_authors><pubmed_authors>Berthel E</pubmed_authors><pubmed_authors>Bodgi L</pubmed_authors><pubmed_authors>Devic C</pubmed_authors><pubmed_authors>Pereira S</pubmed_authors><pubmed_authors>Ferlazzo ML</pubmed_authors><pubmed_authors>Charlet L</pubmed_authors><pubmed_authors>Sonzogni L</pubmed_authors><pubmed_authors>Foray N</pubmed_authors><pubmed_authors>Granzotto A</pubmed_authors></additional><is_claimable>false</is_claimable><name>DNA Double-Strand Breaks Induced in Human Cells by Twelve Metallic Species: Quantitative Inter-Comparisons and Influence of the ATM Protein.</name><description>Despite a considerable amount of data, the molecular and cellular bases of the toxicity due to metal exposure remain unknown. Recent mechanistic models from radiobiology have emerged, pointing out that the radiation-induced nucleo-shuttling of the ATM protein (RIANS) initiates the recognition and the repair of DNA double-strand breaks (DSB) and the final response to genotoxic stress. In order to document the role of ATM-dependent DSB repair and signalling after metal exposure, we applied twelve different metal species representing nine elements (Al, Cu, Zn Ni, Pd, Cd, Pb, Cr, and Fe) to human skin, mammary, and brain cells. Our findings suggest that metals may directly or indirectly induce DSB at a rate that depends on the metal properties and concentration, and tissue type. At specific me</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Oct</publication><modification>2025-04-21T21:59:13.763Z</modification><creation>2025-04-21T21:59:13.763Z</creation></dates><accession>S-EPMC8533583</accession><cross_references><pubmed>34680095</pubmed><doi>10.3390/biom11101462</doi></cross_references></HashMap>