Polycyclic aromatic hydrocarbons-enriched diesel exhaust particles induced hypertrophy in rat primary neonatal cardiomyocytes and apoptotic cell death in H9c2 cardiomyocytes.
Journal
Toxicology
ISSN
1879-3185
Date Issued
2026-01-01
Author(s)
Abstract
There is limited research about the direct effects of diesel exhaust particles (DEPs) on cardiomyocytes. The respirable DEPs asorbed many organic substances such as polycyclic aromatic hydrocarbons (PAHs). Here, we used the standard DEPs, enriched in PAHs and their derivatives, from the National Institute of Standards and Technology of the United States and extracted the organic compounds of DEPs (DEPEs) to examine the effects and mechanisms of DEPEs on rat primary neonatal cardiomyocytes (NRCMs) and rat embryonic H9c2 cardiomyocytes. No cytotoxicity was found at DEPEs concentrations up to 25μg/mL in NRCMs. By evidence of immunofluorescence of desmin, cellular protein content, and mRNA levels of brain natriuretic peptide and β-myosin heavy chain, the cell hypertrophy was induced by DEPEs in NRCMs. DEPEs induced cytotoxicity in H9c2 cells at the concentration of 15μg/mL and up. DEPEs exposure significantly induced apoptosis and protein expression of phosphorylated JNK and endoplasmic reticulum stress markers glucose-regulated protein 78 and C/EBP-homologous protein in H9c2 cells. Altogether, the direct effects of PAHs-enriched DEPEs include cytotoxic effects observed in H9c2 cells at higher concentrations and hypertrophic effects in NRCMs at concentrations without cytotoxicity. These results provide the better understanding of direct effects of DEPs on cardiomyocytes.
Subjects
cardiotoxicity
diesel exhaust particles
endoplasmic reticulum stress
hypertrophy
Type
journal article