Morphological and Physicochemical Characterization of Agglomerates of Titanium Dioxide Nanoparticles in Cell Culture Media

Titanium dioxide nanoparticles (TiO2 NP) are possible carcinogenic materials (2B-IARC) and their toxicity depends on shape, size, and electrical charge of primary NP and on the system formed by NP media. The aim of this work was to characterize agglomerates of three TiO2 NP by evaluating their morphometry, stability, and zeta potential (ζ) in liquid media and their changes with time. Sizes of agglomerates by dynamic light scattering (DLS) resulted to be 10–50 times larger than those obtained by digital image analysis (DIA) given the charged zone around particles. Fractal dimension (FD) was highest for agglomerates of spheres and belts in F12K, and in E171 in FBS media. E171 and belts increased FD with time. At time zero, using water as dispersant FD was larger for agglomerates of spheres than for of E171. Belts suspended in water had the smallest values of circularity (Ci) which was approximately unchanged with time. All dispersions had ζ values around −30 mV at physiological pH (7.4) and dispersions of NP in water and FBS showed maximum stability (Turbiscan Lab analysis). Results help in understanding the complex NP geometry-size-stability relationships when performing in vivo and in vitro environmental-toxicity works and help in supporting decisions on the usage of TiO2 NP

Zinc Oxide Nanoparticles Induce Toxicity in H9c2 Rat Cardiomyoblasts

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