Zinc oxide nanoparticles (ZnO NPs) are widely used in the cosmetic industry. They are nano-optical and nano-electrical devices, and their antimicrobial properties are applied in food packaging and medicine. ZnO NPs penetrate the body through inhalation, oral, and dermal exposure and spread through circulation to various systems and organs. Since the cardiovascular system is one of the most vulnerable systems, in this work, we studied ZnO NPs toxicity in H9c2 rat cardiomyoblasts. Cardiac cells were exposed to different concentrations of ZnO NPs, and then the morphology, proliferation, viability, mitochondrial membrane potential (ΔΨm), redox state, and protein expression were measured. Transmission electron microscopy (TEM) and hematoxylin–eosin (HE) staining showed strong morphological damage. ZnO NPs were not observed inside cells, suggesting that Zn2+ ions were internalized, causing the damage. ZnO NPs strongly inhibited cell proliferation and MTT reduction at 10 and 20 μg/cm2 after 72 h of treatment. ZnO NPs at 20 μg/cm2 elevated DCF fluorescence, indicating alterations in the cellular redox state associated with changes in ΔΨm and cell death. ZnO NPs also reduced the intracellular expression of troponin I and atrial natriuretic peptide. ZnO NPs are toxic for cardiac cells; therefore, consumption of products containing them could cause heart damage and the development of cardiovascular diseases.
Background Zinc oxide nanoparticles (ZnO NPs) are widely used in the cosmetic industry. They are nano-optical and nano-electrical devices, and their antimicrobial properties are applied in food packaging and medicine. ZnO NPs penetrate the body by inhalation, oral and dermal exposure and spread through circulation to various systems and organs. Since the cardiovascular system is one of the most vulnerable ones, in this work we studied ZnO NPs toxicity in H9c2 rat cardiomyoblasts. Methods Cardiac cells were exposed to different concentrations of ZnO NPs and then measured morphology, proliferation, viability, mitochondrial membrane potential (ΔΨm), redox state and protein expression. Results Transmission electronic microscopy (TEM) and hematoxylin/eosin (H/E) staining showed strong morphological damage. ZnO NPs were not observed inside cells, suggesting Zn2+ ions were internalized, causing the damage. ZnO NPs strongly inhibited cell proliferation and MTT reduction at 10 and 20 µg/cm2 after 72 h of treatment. ZnO NPs at 20 µg/cm2 elevated DCF fluorescence indicating alterations in cellular redox state, associated with changes in ΔΨm and cell death. ZnO NPs also reduced troponin I and atrial natriuretic peptide expression. Conclusions ZnO NPs are toxic for cardiac cells, therefore consumption of products containing them could cause heart damage and develop cardiovascular diseases.
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