Fig. 4From: Amorphous SiO2 nanoparticles promote cardiac dysfunction via the opening of the mitochondrial permeability transition pore in rat heart and human cardiomyocytesnanoSiO2 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 proteinsBack to article page