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Background <p>Epidemiological studies suggest an association between air pollution and ventricular arrhythmias, with reactive oxygen species (ROS) playing a crucial role. However, the causal relationship and long-term effects remain uncertain, and the effectiveness of interventions aimed at reducing ROS requires further investigation. Here we aimed to evaluate the effects of a 3-weeks exposure to diesel exhaust particles (DEPs) on ventricular arrhythmogenesis, explore the underlying mechanisms, and assess the potential of cerium oxide nanoparticles (CeO<sub>2</sub>NP) as a ROS-detoxifying intervention.</p> Results <p>Sprague–Dawley rats underwent intratracheal instillation of saline without or with DEPs (7.5&#xa0;g/Kg for 1–3&#xa0;weeks). Ventricular arrhythmia inducibility was then assessed in isolated hearts using a protocol of programmed electrical stimulation. Cardiac hypertrophy, collagen content, inflammation and oxidative stress were analyzed using histology, Western blot, RT-qPCR, and measurement of malondialdehyde content. The potential protective effects of CeO<sub>2</sub>NP (0.5&#xa0;mg/Kg/week, i.p.) were also tested. DEP exposure for 3&#xa0;weeks increased the incidence and duration of sustained ventricular tachyarrhythmias (VTs), a finding that correlated with a moderate increase in interstitial collagen (from 3.11 ± 0.12% in controls to 4.80 ± 0.21% in DEP-exposed rats, p &lt; 0.001), and an early upregulation in the expression of collagen and other fibrotic and inflammatory markers. These effects associated with prolonged QRS complex and enhanced malondialdehyde content (356.7 ± 21.2 vs. 455.3 ± 17.2 μmol/g tissue, p = 0.0066) after 3&#xa0;weeks. CeO<sub>2</sub>NP treatment reduced oxidative stress and myocardial fibrosis, reversed electrocardiographic changes and attenuated DEP-induced pro-arrhythmic effects.</p> Conclusions <p>DEP exposure increases the incidence and duration of sustained VTs, collagen deposition and oxidative stress in rats. Treatment with CeO<sub>2</sub>NP attenuate these effects, arising as a potential novel strategy to mitigate the deleterious effects of air pollution.</p>

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Insights into the causal role of diesel exhaust particles in ventricular arrhythmogenesis: protective effects of antioxidant cerium oxide nanoparticles

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月25日

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  • Freddy G. Ganse,
  • Lena M. Ernst,
  • Cristina Rodríguez,
  • Marisol Ruiz-Meana,
  • Javier Inserte,
  • José Martínez-González,
  • Ana M. Briones,
  • Ana Belén García-Redondo,
  • Marta Consegal,
  • Elisabet Miró-Casas,
  • Laia Yáñez-Bisbe,
  • Aitor Pomposo,
  • Marta Prades-Martínez,
  • Ignacio Ferreira-González,
  • Victor Puntes,
  • Begoña Benito,
  • Antonio Rodríguez-Sinovas

摘要

Background

Epidemiological studies suggest an association between air pollution and ventricular arrhythmias, with reactive oxygen species (ROS) playing a crucial role. However, the causal relationship and long-term effects remain uncertain, and the effectiveness of interventions aimed at reducing ROS requires further investigation. Here we aimed to evaluate the effects of a 3-weeks exposure to diesel exhaust particles (DEPs) on ventricular arrhythmogenesis, explore the underlying mechanisms, and assess the potential of cerium oxide nanoparticles (CeO2NP) as a ROS-detoxifying intervention.

Results

Sprague–Dawley rats underwent intratracheal instillation of saline without or with DEPs (7.5 g/Kg for 1–3 weeks). Ventricular arrhythmia inducibility was then assessed in isolated hearts using a protocol of programmed electrical stimulation. Cardiac hypertrophy, collagen content, inflammation and oxidative stress were analyzed using histology, Western blot, RT-qPCR, and measurement of malondialdehyde content. The potential protective effects of CeO2NP (0.5 mg/Kg/week, i.p.) were also tested. DEP exposure for 3 weeks increased the incidence and duration of sustained ventricular tachyarrhythmias (VTs), a finding that correlated with a moderate increase in interstitial collagen (from 3.11 ± 0.12% in controls to 4.80 ± 0.21% in DEP-exposed rats, p < 0.001), and an early upregulation in the expression of collagen and other fibrotic and inflammatory markers. These effects associated with prolonged QRS complex and enhanced malondialdehyde content (356.7 ± 21.2 vs. 455.3 ± 17.2 μmol/g tissue, p = 0.0066) after 3 weeks. CeO2NP treatment reduced oxidative stress and myocardial fibrosis, reversed electrocardiographic changes and attenuated DEP-induced pro-arrhythmic effects.

Conclusions

DEP exposure increases the incidence and duration of sustained VTs, collagen deposition and oxidative stress in rats. Treatment with CeO2NP attenuate these effects, arising as a potential novel strategy to mitigate the deleterious effects of air pollution.