Amorphous SiO2 nanoparticles promote cardiac dysfunction via the opening of the mitochondrial permeability transition pore in rat heart and human cardiomyocytes

Lozano, Omar; Silva-Platas, Christian; Chapoy‐Villanueva, Héctor; Pérez-Benítez, Baruc Emet; Lees, Jarmon G.; Ramachandra, Chrishan J A; Contreras‐Torres, Flavio F.; Lázaro‐Alfaro, Anay; Luna-Figueroa, Estefanía; Bernal‐Ramírez, Judith; Gordillo-Galeano, Aldemar; Benítez, Alfredo; Oropeza-Almazán, Yuriana; Castillo, Elena C.; Koh, Poh Ling; Hausenloy, Derek J.; Lim, Shiang Y.; García‐Rivas, Gerardo

doi:10.1186/s12989-020-00346-2

Cited by 34 publications

(18 citation statements)

References 61 publications

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“…1C), the remarkable structural impairments on cardiac mitochondria upon SiNPs exposure implied the prominent role of mitochondrial-associated oxidative stress and mitochondrial dysfunction in cardiac disorders caused by SiNPs. Consistently, studies have shown the induction of mitochondrial dysfunction by SiNPs in cardiomyocytes, 30,37 as evidenced by the declined mitochondrial membrane potential and ATP content and increased ROS production, leading to the impaired cardiac function. But the interactions between SiNPs and cardiomyocytes or their organelle ( e.g.…”

Section: Discussionsupporting

confidence: 61%

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Myocardial toxicity induced by silica nanoparticles in a transcriptome profile

Zhao

et al. 2022

Nanoscale

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Section: Discussionsupporting

confidence: 61%

“…29 In vivo data have provided the induction of myocardial injury, particularly myocar- dial contractile dysfunction in rats by repeated SiNPs exposure (a one-month period) via intratracheal instillation. 20,30,31 However, the potential underlying mechanisms remain incompletely elucidated.…”

Section: Discussionmentioning

confidence: 99%

Myocardial toxicity induced by silica nanoparticles in a transcriptome profile

Zhao

et al. 2022

Nanoscale

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“…Alternative studies have indicated that SiNPs (i) induce cardiac dysfunction and bradycardia via the neutrophil-mediated cardiac inflammation in zebrafish embryos, 16 (ii) exert toxic effect on isolated adult cardiomyocytes via impairment of mitochondrial function and Ca 2+ homeostasis, 19 and (iii) induce cardiac dysfunction via the opening of the mitochondrial permeability transition pore in rat heart and human cardiomyocytes. 28 These findings suggest that dysfunction of mitochondria and Ca 2+ homeostasis in cardiomyocytes and myocardial inflammation plays important role in the cardiac toxicity of SiNPs. The present study further demonstrated that the hazardous effects of SiNPs on several ion channels and AP are also important mechanisms underlying the arrhythmogenic effects of SiNPs.…”

Section: Discussionmentioning

confidence: 96%

<p>Silica Nanoparticles Disturb Ion Channels and Transmembrane Potentials of Cardiomyocytes and Induce Lethal Arrhythmias in Mice</p>

Liu¹,

Xue²,

Zhang³

et al. 2020

IJN

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Background: The toxicity of silica nanoparticles (SiNPs) on cardiac electrophysiology has seldom been evaluated. Methods: Patch-clamp was used to investigate the acute effects of SiNP-100 (100 nm) and SiNP-20 (20 nm) on the transmembrane potentials (TMPs) and ion channels in cultured neonatal mouse ventricular myocytes. Calcium mobilization in vitro, cardiomyocyte ROS generation, and LDH leakage after exposure to SiNPs in vitro and in vivo were measured using a microplate reader. Surface electrocardiograms were recorded in adult mice to evaluate the arrhythmogenic effects of SiNPs in vivo. SiNP endocytosis was observed using transmission electron microscopy. Results: Within 30 min, both SiNPs (10 −8-10 −6 g/mL) did not affect the resting potential and I K1 channels. SiNP-100 increased the action potential amplitude (APA) and the I Na current density, but SiNP-20 decreased APA and I Na density. SiNP-100 prolonged the action potential duration (APD) and decreased the I to current density, while SiNP-20 prolonged or shortened the APD, depending on exposure concentrations and increased I to density. Both SiNPs (10 −6 g/mL) induced calcium mobilization but did not increase ROS and LDH levels and were not endocytosed within 10 min in cardiomyocytes in vitro. In vivo, SiNP-100 (4-10 mg/kg) and SiNP-20 (4-30 mg/kg) did not elevate myocardial ROS but increased LDH levels depending on dose and exposure time. The same higher dose of SiNPs (intravenously injected) induced tachyarrhythmias and lethal bradyarrhythmias within 90 min in adult mice. Conclusion: SiNPs (i) exert rapid toxic effects on the TMPs of cardiomyocytes in vitro largely owing to their direct interfering effects on the I Na and I to channels and Ca 2+ homeostasis but not I K1 channels and ROS levels, and (ii) induce tachyarrhythmias and lethal bradyarrhythmias in vivo. SiNP-100 is more toxic than SiNP-20 on cardiac electrophysiology, and the toxicity mechanism is likely more complicated in vivo.

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“…Silica nanoparticles induce cardiac dysfunction in rat hearts and human cardiomyocytes [ 188 ] and cardiotoxicity in adult rat cardiomyocytes [ 189 ]. Silica nanoparticles disturb ion channels and transmembrane potentials in cardiomyocytes and induce arrhythmias in adult male C57BL/6J mice [ 190 ].…”

Section: Autophagy-related Responses To Mss and Nss In Animal And Cell Linesmentioning

confidence: 99%

Micro- and Nanosized Substances Cause Different Autophagy-Related Responses

Wang

Zheng

Lee

et al. 2021

IJMS

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With rapid industrialization, humans produce an increasing number of products. The composition of these products is usually decomposed. However, some substances are not easily broken down and gradually become environmental pollutants. In addition, these substances may cause bioaccumulation, since the substances can be fragmented into micro- and nanoparticles. These particles or their interactions with other toxic matter circulate in humans via the food chain or air. Whether these micro- and nanoparticles interfere with extracellular vesicles (EVs) due to their similar sizes is unclear. Micro- and nanoparticles (MSs and NSs) induce several cell responses and are engulfed by cells depending on their size, for example, particulate matter with a diameter ≤2.5 μm (PM2.5). Autophagy is a mechanism by which pathogens are destroyed in cells. Some artificial materials are not easily decomposed in organisms. How do these cells or tissues respond? In addition, autophagy operates through two pathways (increasing cell death or cell survival) in tumorigenesis. Many MSs and NSs have been found that induce autophagy in various cells and tissues. As a result, this review focuses on how these particles interfere with cells and tissues. Here, we review MSs, NSs, and PM2.5, which result in different autophagy-related responses in various tissues or cells.

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Amorphous SiO2 nanoparticles promote cardiac dysfunction via the opening of the mitochondrial permeability transition pore in rat heart and human cardiomyocytes

Cited by 34 publications

References 61 publications

Myocardial toxicity induced by silica nanoparticles in a transcriptome profile

Myocardial toxicity induced by silica nanoparticles in a transcriptome profile

<p>Silica Nanoparticles Disturb Ion Channels and Transmembrane Potentials of Cardiomyocytes and Induce Lethal Arrhythmias in Mice</p>

Micro- and Nanosized Substances Cause Different Autophagy-Related Responses

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