Nano-titanium dioxide (TiO2) is one of the most commonly used materials being synthesized for use as one of the top five nanoparticles. Due to the extensive application of TiO2 nanoparticles and their inclusion in many commercial products, the increased exposure of human beings to nanoparticles is possible. This exposure could be routed via dermal penetration, inhalation and oral ingestion or intravenous injection. Therefore, regular evaluation of their potential toxicity and distribution in the bodies of exposed individuals is essential. Keeping in view the potential health hazards of TiO2 nanoparticles for humans, we reviewed the research articles about studies performed on rats or other mammals as animal models. Most of these studies utilized the dermal or skin and the pulmonary exposures as the primary routes of toxicity. It was interesting that only very few studies revealed that the TiO2 nanoparticles could penetrate through the skin and translocate to other tissues, while many other studies demonstrated that no penetration or translocation could happen through the skin. Conversely, the TiO2 nanoparticles that entered through the pulmonary route were translocated to the brain or the systemic circulation from where these reached other organs like the kidney, liver, etc. In most studies, TiO2 nanoparticles appeared to have caused oxidative stress, histopathological alterations, carcinogenesis, genotoxicity and immune disruption. Therefore, the use of such materials in humans must be either avoided or strictly managed to minimise risks for human health in various situations.

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Background and Purpose Recently, a novel locus at 17q25 was associated with white matter hyperintensities (WMH) on MRI in stroke-free individuals. We aimed to replicate the association with WMH volume (WMHV) in patients with ischemic stroke. If the association acts by promoting a small vessel arteriopathy, it might be expected to also associate with lacunar stroke. Methods We quantified WMH on MRI in the stroke-free hemisphere of 2588 ischemic stroke cases. Association between WMHV and 6 single-nucleotide polymorphisms at chromosome 17q25 was assessed by linear regression. These single-nucleotide polymorphisms were also investigated for association with lacunar stroke in 1854 cases and 51 939 stroke-free controls from METASTROKE. Meta-analyses with previous reports and a genetic risk score approach were applied to identify other novel WMHV risk variants and uncover shared genetic contributions to WMHV in community participants without stroke and ischemic stroke. Results Single-nucleotide polymorphisms at 17q25 were associated with WMHV in ischemic stroke, the most significant being rs9894383 (P=0.0006). In contrast, there was no association between any single-nucleotide polymorphism and lacunar stroke. A genetic risk score analysis revealed further genetic components to WMHV shared between community participants without stroke and ischemic stroke. Conclusions This study provides support for an association between the 17q25 locus and WMH. In contrast, it is not associated with lacunar stroke, suggesting that the association does not act by promoting small-vessel arteriopathy or the same arteriopathy responsible for lacunar infarction.

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Silver nanoparticles (17.78 ± 12.12 nm) were synthesized by the reduction of 0.5 M silver nitrate using formaldehyde as reducing and triethylamine as promoting and stabilizing agent. The particles were grain like agglomerates with spherical, centered-face cubic and crystalline in nature. The sample was highly pure with amine (NH) as associated and capping molecules. Further, the genotoxicity and oxidative stress of these particles were evaluated using Labeo rohita (L. rohita) as genetic model exposed (10-55 mg L -1 dose) through aquatic medium for 28 days. The cells were produced with micronuclei, fragmented, lobed and buds nuclei in dose dependent manner. The highest incidence of comet was recoded (27.34 ± 5.68) at 55 mg L -1 Ag-NPs and 14 days treatment. Then frequency was decreased to 22.65 ± 6.66% after 28 days due to complex repair mechanism. Moreover, the treatment also produces the oxidative stress and disturbs the level of GST in gill and liver tissue. There was a sharp decline in the activities of GST and this decrease of activity increase the MDA content. Further, the elevated level of GSH represents that the liver has started defensive mechanism against oxyraidcals. This study concluded, Ag-NPs are genotoxic in nature and produce micronuclei, comet cells and also induces oxidative stress in aquatic organisms.