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

ABSTRACT:

Background

Silica nanoparticles (nanoSiO₂) are promising systems that can deliver biologically active compounds to tissues such as the heart in a controllable manner. However, cardiac toxicity induced by nanoSiO₂ has been recently related to abnormal calcium handling and energetic failure in cardiomyocytes. Moreover, the precise mechanisms underlying this energetic debacle remain unclear. In order to elucidate these mechanisms, this article explores the ex vivo heart function and mitochondria after exposure to nanoSiO₂.

Results

The cumulative administration of nanoSiO₂ reduced the mechanical performance index of the rat heart with a half-maximal inhibitory concentration (IC₅₀) of 93 μg/mL, affecting the relaxation rate.

SUBMITTER: Lozano O 

PROVIDER: S-EPMC7206702 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature