<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>11(21)</volume><submitter>Tulen CBM</submitter><funding>This research is supported by the Netherlands Food and Consumer Product Safety Authority (NVWA).</funding><pubmed_abstract>Chronic obstructive pulmonary disease (COPD) is a devastating lung disease primarily caused by exposure to cigarette smoke (CS). During the pyrolysis and combustion of tobacco, reactive aldehydes such as acetaldehyde, acrolein, and formaldehyde are formed, which are known to be involved in respiratory toxicity. Although CS-induced mitochondrial dysfunction has been implicated in the pathophysiology of COPD, the role of aldehydes therein is incompletely understood. To investigate this, we used a physiologically relevant in vitro exposure model of differentiated human primary bronchial epithelial cells (PBEC) exposed to CS (one cigarette) or a mixture of acetaldehyde, acrolein, and formaldehyde (at relevant concentrations of one cigarette) or air, in a continuous flow system using a puff-lik</pubmed_abstract><journal>Cells</journal><pagination>3481</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9655975</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Smoking-Associated Exposure of Human Primary Bronchial Epithelial Cells to Aldehydes: Impact on Molecular Mechanisms Controlling Mitochondrial Content and Function.</pubmed_title><pmcid>PMC9655975</pmcid><pubmed_authors>Dentener MA</pubmed_authors><pubmed_authors>Kloosterboer N</pubmed_authors><pubmed_authors>Opperhuizen A</pubmed_authors><pubmed_authors>Remels AHV</pubmed_authors><pubmed_authors>Fokkens PHB</pubmed_authors><pubmed_authors>Weibolt N</pubmed_authors><pubmed_authors>Koene EJC</pubmed_authors><pubmed_authors>Jessen PJJ</pubmed_authors><pubmed_authors>Cremers JWJM</pubmed_authors><pubmed_authors>Staal YCM</pubmed_authors><pubmed_authors>van Schooten FJ</pubmed_authors><pubmed_authors>Tulen CBM</pubmed_authors><pubmed_authors>Klerx WNM</pubmed_authors><pubmed_authors>Maas L</pubmed_authors><pubmed_authors>Duistermaat E</pubmed_authors><pubmed_authors>Gremmer ER</pubmed_authors></additional><is_claimable>false</is_claimable><name>Smoking-Associated Exposure of Human Primary Bronchial Epithelial Cells to Aldehydes: Impact on Molecular Mechanisms Controlling Mitochondrial Content and Function.</name><description>Chronic obstructive pulmonary disease (COPD) is a devastating lung disease primarily caused by exposure to cigarette smoke (CS). During the pyrolysis and combustion of tobacco, reactive aldehydes such as acetaldehyde, acrolein, and formaldehyde are formed, which are known to be involved in respiratory toxicity. Although CS-induced mitochondrial dysfunction has been implicated in the pathophysiology of COPD, the role of aldehydes therein is incompletely understood. To investigate this, we used a physiologically relevant in vitro exposure model of differentiated human primary bronchial epithelial cells (PBEC) exposed to CS (one cigarette) or a mixture of acetaldehyde, acrolein, and formaldehyde (at relevant concentrations of one cigarette) or air, in a continuous flow system using a puff-lik</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2025-04-25T23:40:25.681Z</modification><creation>2025-04-06T09:23:05.992Z</creation></dates><accession>S-EPMC9655975</accession><cross_references><pubmed>36359877</pubmed><doi>10.3390/cells11213481</doi></cross_references></HashMap>