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Fig. 4 | Particle and Fibre Toxicology

Fig. 4

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

Fig. 4

nanoSiO2 disturbs mitochondrial enzymatic activity and promote the oxidation of mitochondrial proteins. MitoTEMPO, a mitochondrial antioxidant, partially prevents nanoSiO2 oxidation effects. a Representative recordings of mitochondrial calcium transport in nanoSiO2 (30 μg/mL) incubated in mitochondria after the addition of 10 μM Ca2+. MitoTEMPO improved mitochondrial calcium transport. b Aconitase enzyme activity, c free thiol content, and d mitochondrial thiols in the ANT interlinked by n-ethylmaleimide (NEM) binding in isolated heart mitochondria after nanoSiO2 treatment (30 μg/mL) in presence or absence of MitoTEMPO (25 μM). The exposure of mitochondria to nanoSiO2 was 5 min prior to measurements. MitoTEMPO was applied 30 min prior to nanoSiO2 administration. Values are percentage of control and represent mean ± SEM. *p ≤ 0.05 vs control, #p ≤ 0.05 vs SNP. e Schematic interaction of NEM with SH groups in proteins

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