Impact of sub-acute acrolein inhalation on the molecular regulation of mitochondrial metabolism in rat lung.

Autor: Tulen CBM; School of Nutrition and Translational Research in Metabolism (NUTRIM), Department of Pharmacology and Toxicology, Maastricht University Medical Center+, Maastricht, the Netherlands., Leermakers PA; School of Nutrition and Translational Research in Metabolism (NUTRIM), Department of Pharmacology and Toxicology, Maastricht University Medical Center+, Maastricht, the Netherlands., Schrieder SE; School of Nutrition and Translational Research in Metabolism (NUTRIM), Department of Pharmacology and Toxicology, Maastricht University Medical Center+, Maastricht, the Netherlands., van Schooten FJ; School of Nutrition and Translational Research in Metabolism (NUTRIM), Department of Pharmacology and Toxicology, Maastricht University Medical Center+, Maastricht, the Netherlands., Opperhuizen A; School of Nutrition and Translational Research in Metabolism (NUTRIM), Department of Pharmacology and Toxicology, Maastricht University Medical Center+, Maastricht, the Netherlands; Netherlands Food and Consumer Product Safety Authority (NVWA), Utrecht, the Netherlands., Remels AHV; School of Nutrition and Translational Research in Metabolism (NUTRIM), Department of Pharmacology and Toxicology, Maastricht University Medical Center+, Maastricht, the Netherlands. Electronic address: a.remels@maastrichtuniversity.nl.
Jazyk: angličtina
Zdroj: Toxicology letters [Toxicol Lett] 2023 Apr 01; Vol. 378, pp. 19-30. Date of Electronic Publication: 2023 Feb 16.
DOI: 10.1016/j.toxlet.2023.02.003
Abstrakt: Nowadays, mitochondria are recognized as key players in the pathogenesis of a variety of smoking-associated lung diseases. Acrolein, a component of cigarette smoke, is a known driver of biological mechanisms underlying smoking-induced respiratory toxicity. The impact of sub-acute acrolein inhalation in vivo on key processes controlling mitochondrial homeostasis in cells of the airways however is unknown. In this study, we investigated the activity/abundance of a myriad of molecules critically involved in mitochondrial metabolic pathways and mitochondrial quality control processes (mitochondrial biogenesis and mitophagy) in the lungs of Sprague-Dawley rats that were sub-acutely exposed to filtered air or 3 ppm acrolein by whole-body inhalation (5 h/day, 5 days/week for 4 weeks). Acrolein exposure induced a general inflammatory response in the lung as gene expression analysis revealed an increased expression of Icam1 and Cinc1 (p < 0.1; p < 0.05). Acrolein significantly decreased enzyme activity of hydroxyacyl-Coenzyme A dehydrogenase (p < 0.01), and decreased Pdk4 transcript levels (p < 0.05), suggestive of acrolein-induced changes in metabolic processes. Investigation of constituents of the mitochondrial biogenesis pathways and mitophagy machinery revealed no pronounced alterations. In conclusion, sub-acute inhalation of acrolein did not affect the regulation of mitochondrial metabolism and quality control, which is in contrast to more profound changes after acute exposure in other studies.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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