Different dermal cell types have been reported to differ in their sensitivity to nano-sized TiO₂ . Kiss et al. exposed human keratinocytes (HaCaT), human dermal fibroblast cells, sebaceous gland cells (SZ95) and primary human melanocytes to 9 nm-sized TiO₂ particles at concentrations from 0.15 to 15 μg/cm² for up to 4 days. The particles were detected in the cytoplasm and perinuclear region in fibroblasts and melanocytes, but not in kerati-nocytes or sebaceous cells. The uptake was associated with an increase in the intracellular Ca²⁺ concentration. A dose- and time-dependent decrease in cell proliferation was evident in all cell types, whereas in fibroblasts an increase in cell death via apoptosis has also been observed. Anatase TiO₂ in 20–100 nm-sized form has been shown to be cytotoxic in mouse L929 fibroblasts. The decrease in cell viability was associated with an increase in the production of ROS and the depletion of glutathione. The particles were internalized and detected within lysosomes. In human keratinocytes exposed for 24 h to non-illuminated, 7 nm-sized anatase TiO_2, a cluster analysis of the gene expression revealed that genes involved in the “inflammatory response” and “cell adhesion”, but not those involved in “oxidative stress” and “apoptosis”, were up-regulated. The results suggest that non-illuminated TiO₂ particles have no significant impact on ROS-associated oxidative damage, but affect the cell-matrix adhesion in keratinocytes in extracellular matrix remodelling. In human keratinocytes, Kocbek et al. investigated the adverse effects of 25 nm-sized anatase TiO₂ (5 and 10 μg/ml) after 3 months of exposure and found no changes in the cell growth and morphology, mitochondrial function and cell cycle distribution. The only change was a larger number of nanotubular intracellular connections in TiO₂-exposed cells compared to non-exposed cells. Although the authors proposed that this change may indicate a cellular transformation, the significance of this finding is not clear. On the other hand, Dunford et al. studied the genotoxicity of UV-irradiated TiO₂ extracted from sunscreen lotions, and reported severe damage to plasmid and nuclear DNA in human fibroblasts. Manitol (antioxidant) prevented DNA damage, implying that the genotoxicity was mediated by ROS.

Rutile Titanium Dioxide (TiO2) is one of the most widely used and versatile materials in various industries, particularly in coatings and plastics. As a leading supplier of MBR9668, a specialized rutile titanium dioxide coating, companies are empowered to enhance the performance and durability of their products significantly. This article explores the unique properties of MBR9668 and its applications across diverse sectors.

Both calcium carbonate and titanium dioxide play crucial roles in various industries, but they are used for different purposes. Calcium carbonate is primarily used as a filler and pigment, while titanium dioxide is used as a whitening agent and pigment. Additionally, titanium dioxide is more expensive to produce than calcium carbonate due to its synthetic nature and complex manufacturing process.

The realization of neuromorphic resistive memory in TiO₂ thin films (Strukov et al., 2008) marked an important milestone in the search for bio-inspired technologies (Chua and Kang, 1976). Many research proposals urged a focus on memristivity as the common feature of two electrical models: (i) electromigration of point defects in titanium oxide systems (Baiatu et al., 1990; Jameson et al., 2007) and (ii) voltage-gated ionic channels in the membranes of biological neurons (Hodgkin and Huxley, 1952). In this regard, memristors functionally mimic the synaptic plasticity of biological neurons, and thus can be implemented in artificial and hybrid neural networks. This includes a new paradigm of future computing systems (Zidan, 2018) and biocompatible electronics such as biointerfaces and biohybrid systems (Chiolerio et al., 2017).

No acute effects of nano-sized TiO₂ were observed in Danio rerio (zebrafish) embryos. Exposure of rainbow trout to TiO₂ NPs triggered lipid peroxidation, influence on the respiratory tract, disturbance in the metabolism of Cu and Zn, induction of intestinal erosion  and accumulation in kidney tissue. Linhua et al. exposed juvenile carp to 100 and 200 mg/ml of particles and TiO₂ observed no mortality. However, the fish suffered from oxidative stress and pathological changes in gill and liver. In the infaunal species Arenicola marina, exposure to TiO₂ NPs in sediment caused sub-lethal effects including decrease in casting rate and increase in cellular and DNA damage. Aggregated particles were visible in the lumen of the gut, but no uptake through the gut or the skin was observed.