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Peer-reviewedCC BY 4.0Biomolecules

Diesel Exhaust Particles Exposure Disrupts Cardiac Bioenergetics and Induces a Shift Towards Glycolytic Metabolism in Rats

  • Freddy G. Ganse1,2
  • Marta Consegal1,2
  • Cristina Rodríguez2,3
  • Elisabet Miró-Casas1,2
  • Marisol Ruiz-Meana1,2
  • Javier Inserte1,2
  • José Martínez-González2,3,4
  • Ignacio Ferreira-González1,5
  • Begoña Benito1,2
  • Antonio Rodríguez-Sinovas1,2
5 affiliations
  1. 1Cardiovascular Diseases Research Group, Vall d’Hebron Institute of Research (VHIR) and Universitat Autònoma de Barcelona, Instituto de Investigación Sanitaria Hospital Universitario Vall d’Hebron (IIS IR-HUVH), 08035 Barcelona, Spain
  2. 2CIBER de Enfermedades Cardiovasculares (CIBERCV), Instituto de Salud Carlos III (ISCIII), 28029 Madrid, Spain
  3. 3Institut de Recerca Sant Pau (IR SANT PAU), 08041 Barcelona, Spain
  4. 4Instituto de Investigaciones Biomédicas de Barcelona-Consejo Superior de Investigaciones Científicas (IIBB-CSIC), 08036 Barcelona, Spain
  5. 5CIBER de Epidemiología y Salud Pública (CIBERESP), Instituto de Salud Carlos III (ISCIII), 28029 Madrid, Spain
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Abstract

Air pollution, particularly particulate matter (PM), is a major contributor to cardiovascular morbidity and mortality. We previously showed that diesel exhaust particles (DEPs) exposure increases arrhythmia susceptibility in rats, associated with myocardial oxidative stress and inflammation. However, the impact of DEPs on myocardial metabolism remains incompletely characterized. Here we aim to investigate whether DEP exposure induces time-dependent alterations in cardiac and plasma metabolic profiles following short- and longer-term intratracheal instillations in rats. Sprague–Dawley rats received intratracheal instillations of DEPs or saline three times weekly for one or three weeks. Myocardial and plasma metabolites were analyzed by 1H nuclear magnetic resonance spectroscopy, followed by discriminant and pathway analyses. Myocardial metabolomic profiling proved supportive of group separation, particularly one week after exposure. Seventeen of 22 metabolites were significantly altered. One week of DEP exposure reduced succinate, acetate, formate, 3-hydroxybutyrate, ATP, and ADP levels, a pattern consistent with alterations in mitochondrial oxidative metabolism and β-oxidation. Increased glucose and lactate levels were consistent with a greater reliance on glycolytic metabolism. Amino acid accumulation, along with increased inosine, pointed towards altered amino acid utilization and enhanced nucleotide degradation. Pathway analyses identified purine metabolism, glycolysis, citrate cycle, and pyruvate metabolism as some of the affected pathways, with enrichment of the citric acid cycle and mitochondrial electron transport chain. Most alterations resolved after three weeks. In contrast, changes in plasma were modest. In conclusion, DEP exposure induces transient metabolic remodeling in the myocardium, characterized by alterations consistent with reduced oxidative metabolism, increased glycolytic reliance, and disruption of energy and redox homeostasis, providing mechanistic insight into pollution-induced cardiac dysfunction.

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Cite

BibTeXRIS
BibTeX
@article{ganse2026diesel,
  title = {{Diesel Exhaust Particles Exposure Disrupts Cardiac Bioenergetics and Induces a Shift Towards Glycolytic Metabolism in Rats}},
  author = {Freddy G. Ganse and Marta Consegal and Cristina Rodríguez and Elisabet Miró-Casas and Marisol Ruiz-Meana and Javier Inserte and José Martínez-González and Ignacio Ferreira-González and Begoña Benito and Antonio Rodríguez-Sinovas},
  journal = {Biomolecules},
  year = {2026},
  month = oct,
  doi = {10.3390/biom16101501},
  url = {https://www.mdpi.com/2218-273X/16/10/1501},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Diesel Exhaust Particles Exposure Disrupts Cardiac Bioenergetics and Induces a Shift Towards Glycolytic Metabolism in Rats
AU  - Freddy G. Ganse
AU  - Marta Consegal
AU  - Cristina Rodríguez
AU  - Elisabet Miró-Casas
AU  - Marisol Ruiz-Meana
AU  - Javier Inserte
AU  - José Martínez-González
AU  - Ignacio Ferreira-González
AU  - Begoña Benito
AU  - Antonio Rodríguez-Sinovas
PY  - 2026
DA  - 2026/10/01
JO  - Biomolecules
DO  - 10.3390/biom16101501
UR  - https://www.mdpi.com/2218-273X/16/10/1501
AB  - Air pollution, particularly particulate matter (PM), is a major contributor to cardiovascular morbidity and mortality. We previously showed that diesel exhaust particles (DEPs) exposure increases arrhythmia susceptibility in rats, associated with myocardial oxidative stress and inflammation. However, the impact of DEPs on myocardial metabolism remains incompletely characterized. Here we aim to investigate whether DEP exposure induces time-dependent alterations in cardiac and plasma metabolic profiles following short- and longer-term intratracheal instillations in rats. Sprague–Dawley rats received intratracheal instillations of DEPs or saline three times weekly for one or three weeks. Myocardial and plasma metabolites were analyzed by 1H nuclear magnetic resonance spectroscopy, followed by discriminant and pathway analyses. Myocardial metabolomic profiling proved supportive of group separation, particularly one week after exposure. Seventeen of 22 metabolites were significantly altered. One week of DEP exposure reduced succinate, acetate, formate, 3-hydroxybutyrate, ATP, and ADP levels, a pattern consistent with alterations in mitochondrial oxidative metabolism and β-oxidation. Increased glucose and lactate levels were consistent with a greater reliance on glycolytic metabolism. Amino acid accumulation, along with increased inosine, pointed towards altered amino acid utilization and enhanced nucleotide degradation. Pathway analyses identified purine metabolism, glycolysis, citrate cycle, and pyruvate metabolism as some of the affected pathways, with enrichment of the citric acid cycle and mitochondrial electron transport chain. Most alterations resolved after three weeks. In contrast, changes in plasma were modest. In conclusion, DEP exposure induces transient metabolic remodeling in the myocardium, characterized by alterations consistent with reduced oxidative metabolism, increased glycolytic reliance, and disruption of energy and redox homeostasis, providing mechanistic insight into pollution-induced cardiac dysfunction.
SN  - 2218-273X
ER  -