ArticleBMC cardiovascular disorders2026
Alumina nanoparticles-induced reduction in Ito, f contributes to the occurrence of ventricular arrhythmias.
Article in BMC cardiovascular disorders, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAluminum 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.
methodsCardiac 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
resultsα-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
conclusionAlumina 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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