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Fig. 6 | Particle and Fibre Toxicology

Fig. 6

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

Fig. 6

nanoSiO2 induces an increase in mitochondrial ROS production, leading to dysfunction in cardiac contractility. Hearts perfused with nanoSiO2 showed a compromised contractility, finding nanoSiO2 accumulation (heart representation, left side). Once nanoSiO2 internalizes into mitochondria, production of ROS is increased, compromising mitochondrial function. This leads to several oxidative damages, reducing the activity of the aconitase, and affecting the activity of key mitochondrial proteins such ANT through the oxidation of thiol groups. ANT oxidation promotes the mPTP formation, causing a decrease in mitochondrial membrane potential, which is the electrochemical force to synthetize ATP, compromising cellular viability. MitoTempo, a mitochondrial antioxidant agent, or CsA through delaying the formation of the mPTP, partially prevented these adverse effects of nanoSiO2 exposure

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Particle and Fibre Toxicology

ISSN: 1743-8977

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