Fig. 5

The toxicity mechanism of nanoSiO₂ in cardiac cells is driven by reactive oxygen species and the opening of the mPTP. a MitoTEMPO dose-dependent cellular death prevention with 200 μg/mL of nanoSiO₂ administration in H9c2 cells. b H₂O₂ production after nanoSiO₂ administration (200 μg/mL) in presence or absence of MitoTEMPO (100 μM) in H9c2 cells. c Cellular viability in ventricular myocytes after nanoSiO₂ administration in the absence or presence of CsA (0.5 μM). d ATP production in cardiomyocytes after nanoSiO₂ administration (100 μg/mL) in absence or presence of CsA (0.5 μM). For human cardiomyocytes: (e) LDH release activity, (f) PI positive cells. MitoTEMPO or CsA were applied 30 min prior to nanoSiO₂ administration. nanoSiO₂ was incubated during 24 h. Values are percentage of control and represent mean ± SEM. *p ≤ 0.05 vs control, #p ≤ 0.05 vs CsA