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Fig. 2 | Particle and Fibre Toxicology

Fig. 2

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

Fig. 2

Exposure to nanoSiO2 to rat and human cardiac mitochondria results in mitochondrial dysfunction, observed by a reduced oxygen consumption rate and mitochondrial membrane potential. For rat cardiomyocyte mitochondria (a-d), at incremental nanoSiO2 concentrations: a Representative recordings of OCR. Addition of succinate and ADP are denoted by arrows. b Decrease of OCR evaluated in state 4 and state 3. c Representative recordings of ΔΨm. Addition of succinate and ADP are denoted by arrows. d Decrease of ΔΨm. For human cardiomyocyte mitochondria, at incremental nanoSiO2 concentrations: e Representative recordings of OCR. Addition of oligomycin, FCCP, rotenone and Antimycin A are denoted by dashed lines. f Basal and maximum OCR, and spare reserve. The exposure of mitochondria to nanoSiO2 was 5 min prior to measurements. Values represent mean ± SEM

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Particle and Fibre Toxicology

ISSN: 1743-8977

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