Alumina nanoparticles-induced reduction in Ito, f contributes to the occurrence of ventricular arrhythmias

Q: What are the key findings of this study?

α-Alumina nanoparticles significantly prolonged QTc intervals to 119.53 ms and reduced Ito,f current density by 81.8%, contributing to the occurrence of ventricular arrhythmias.

Q: What is the clinical evidence from this study?

Population: Ventricular arrhythmias (n=24). Intervention: α-Alumina nanoparticles vs. Double-distilled water. Primary outcome: QTc interval (p=<0.001).

Q: What does this research mean for the field?

α-Alumina nanoparticles induce QT and action potential duration prolongation and promote ventricular arrhythmias through dose-dependent suppression of the cardiac Ito,f current in a crystal phase-dependent manner. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

The study aims to explore the electrophysiological mechanisms and crystal phase-dependent effects of alumina nanoparticles on cardiac function.

Haoze Deng; Mengdie Xia; Yiyang Li; Jie Yang; Xiaodong Qian

doi:10.1186/s12872-026-06250-5

July 11, 2026BMC Cardiovascular DisordersOpen Access

Alumina nanoparticles-induced reduction in Ito, f contributes to the occurrence of ventricular arrhythmias

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Key result

α-Alumina nanoparticles prolong QTc and promote ventricular arrhythmias via an ~82% reduction in Ito,f current.

P<0.001
n=24

Why the study?

Although aluminum oxide nanoparticles induce electrocardiographic abnormalities, their crystal phase-dependent effects and underlying electrophysiological mechanisms remain unclear.

Do α-, γ-, and mix-phase alumina nanoparticles induce QT prolongation, ventricular arrhythmias, and Ito,f current suppression in rat hearts and neonatal rat ventricular myocytes?

Key Points

The study aims to explore the electrophysiological mechanisms and crystal phase-dependent effects of alumina nanoparticles on cardiac function.
Intraperitoneal injection of aluminum oxide nanoparticles in rats at 100 mg/kg.
Exposure of neonatal rat ventricular myocytes to nanoparticle concentrations of 20–100 µg/mL.
Utilization of electrocardiography, monophasic action potential recording, and patch-clamp electrophysiology for analysis.
α-Al₂O₃-NPs prolonged QT intervals by 23.34% (119.53 ± 9.59 ms; p < 0.001).
MAPD₉₀ increased significantly in the α-Al₂O₃-NPs group (187.6 ± 4.9 ms; p < 0.001).
I to, f current density was inhibited by 81.8% at 100 µg/mL of α-Al₂O₃-NPs (p < 0.001).

Structured PICO

Do α-, γ-, and mix-phase alumina nanoparticles induce QT prolongation, ventricular arrhythmias, and Ito,f current suppression in rat hearts and neonatal rat ventricular myocytes?

P

Population

24 male Sprague-Dawley rats and neonatal rat ventricular myocytes were exposed to alumina nanoparticles to assess acute cardiotoxicity and electrophysiological changes.

I

Intervention

Aluminum oxide nanoparticles (Al₂O₃-NPs: α-phase, γ-phase, and mix-phase) administered via single intraperitoneal injection at 100 mg/kg for 90 minutes in adult rats, and in vitro exposure at graded concentrations (20, 50, and 100 µg/mL) for 30 minutes in cultured neonatal rat ventricular myocytes.

C

Comparator

Control group receiving an equal volume of double-distilled (dd) water via intraperitoneal injection in vivo, or untreated vehicle control for in vitro cell exposure.

O

Outcome

QT interval and corrected QT interval (QTc), arrhythmia scores, monophasic action potential duration (MAPD₅₀ and MAPD₉₀), early afterdepolarization (EAD) frequency, and fast transient outward potassium current (Ito,f) density.surrogate

Main Result

Absolute Event Rate: 119.53% vs 96.92%

p-value: p=<0.001

Limitations

The intraperitoneal dose of 100 mg/kg was an acute challenge dose and does not reproduce environmental or occupational human exposure levels.
Intraperitoneal administration was used, which may not reflect pulmonary or gastrointestinal absorption pathways.
In vitro concentrations (20-100 μg/mL) were used for mechanistic evaluation and are not direct equivalents of environmental exposure levels.
In vitro experiments were performed in neonatal rat ventricular myocytes rather than adult cardiomyocytes, which may limit direct extrapolation to the adult heart due to developmental differences in ion channel expression and electrophysiological properties.
The single intraperitoneal dose of 100 mg/kg represents an acute challenge model rather than a direct simulation of real-world human exposure routes such as inhalation, oral ingestion, or dermal contact.
The possibility of artificial toxicity related to acute particle overload, local irritation, osmotic stress, or nonspecific injury cannot be fully excluded.

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Implication

Alumina nanoparticles exhibit crystal phase-dependent cardiotoxicity in rats, with α-Al₂O₃-NPs (but not γ-Al₂O₃-NPs) inducing severe ultrastructural damage, QT and action potential prolongation, and ventricular arrhythmias mediated in part by suppression of the Ito,f potassium current.

Abstract

Aluminum oxide nanoparticles (Al₂O₃-NPs) are currently widely applied, although they are known to induce electrocardiographic abnormalities, their crystal phase-dependent effects (including α- and γ-phases) and underlying electrophysiological mechanisms remain unclear. Cardiac injury of α-, γ-, and mix-phase Al₂O₃-NPs was investigated via intraperitoneal injection (100 mg/kg) in rats and exposure (20–100 µg/mL) in neonatal rat ventricular myocytes (NRVMs). Multidimensional analyses included electrocardiography (ECG), monophasic action potential (MAP) recording, patch-clamp electrophysiology (I to, f current), and transmission electron microscopy (TEM). α-Al₂O₃-NPs significantly prolonged QT intervals (119.53 ± 9.59 ms, increased by 23.34%; p < 0.001) and elevated arrhythmia scores (2.6 ± 0.6 vs. 0 in controls; p < 0.01), whereas γ-Al₂O₃-NPs showed no such effects. The monophasic action potential duration at 90% repolarization (MAPD₉₀) in the α-Al₂O₃-NPs group was 187.6 ± 4.9 ms, which was significantly increased compared with the control group ( p < 0.001). α-Al₂O₃-NPs were found to inhibit I to, f current density in a dose-dependent manner, with a significant reduction of 81.8% observed at 100 µg/mL ( p < 0.001). Ultrastructural damage (myofibril disorganization, mitochondrial cristae fragmentation) and intracellular accumulation of nanoparticles were observed in α-Al₂O₃-NPs group by TEM, with no observed effects for γ-Al₂O₃-NPs. Alumina nanoparticles exhibit crystal phase-dependent cardiotoxicity. α-Al₂O₃-NPs induce QT prolongation, MAPD prolongation, ventricular arrhythmias, and ultrastructural damage in rat hearts. In parallel, α-Al₂O₃-NPs suppress Ito, f currents in cultured neonatal rat ventricular myocytes. These findings suggest that Ito, f inhibition may contribute, to the electrophysiological abnormalities induced by α-Al₂O₃-NPs and provide new insights into the potential mechanisms underlying nanoparticle-induced ventricular arrhythmias.

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Cite This Study

Deng et al. (2026) studied Ventricular arrhythmias (n=24). α-Alumina nanoparticles vs. Double-distilled water was evaluated on QTc interval (p=<0.001). α-Alumina nanoparticles significantly prolonged QTc intervals to 119.53 ms and reduced Ito,f current density by 81.8%, contributing to the occurrence of ventricular arrhythmias.

synapsesocial.com/papers/6a534ff4985393734a594ce7 https://doi.org/10.1186/s12872-026-06250-5

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Alumina nanoparticles-induced reduction in Ito, f contributes to the occurrence of ventricular arrhythmias

Key Points

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Alumina nanoparticles-induced reduction in Ito, f contributes to the occurrence of ventricular arrhythmias

Key Points

Structured PICO

Main Result

Limitations

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

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