Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from mouse liver tissue from SKH:QS mice treated with commercially available sunscreens containing ZnO or TiO2 nanoparticles, or no nanoparticles

ABSTRACT: ZnO and TiO2 nanoparticles can elicit a range of perturbed cell responses in vitro. Exposure to topically applied sunscreens containing ZnO or TiO2 particles may or may not elicit a biological effect in mice. We aimed to compare the biological responses of immune-competent hairless mice receiving topical applications of commercially available sunscreens with or without metal oxide nanoparticles, with the responses of mice receiving no sunscreen. Commercially available sunscreens containing ZnO nanoparticles, a mixture of TiO2 nanoparticles and organic UVR filters, or only organic UVR filters were applied to the backs of SKH:QS mice weekly over 36 weeks, with or without subsequent exposure to 29 kJ/m2 UVR. After 36 weeks and 30 treatments, mice were sacrificed and liver tissue was harvested for RNA isolation and whole genome transcriptional profiling, comparing the expression profiles of treated mice with untreated mice.

ORGANISM(S): Mus musculus

SUBMITTER: Megan Osmond-McLeod

PROVIDER: E-GEOD-84818 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Similar Datasets

Project description:A comprehensive in vitro assessment of two commercial metal oxide nanoparticles, TiO2 and ZnO, was performed using human monocyte-derived macrophages (HMDM), monocyte-derived dendritic cells (MDDC), and T cell leukemia-derived cell line (Jurkat). TiO2 nanoparticles were found to be non-toxic whereas ZnO nanoparticles caused dose-dependent cell death. Subsequently, global gene expression profiling was performed to identify signaling pathways underlying the cytotoxicity caused by ZnO nanoparticles. Analysis was done with doses, 1M-BM-5g/ml and 10M-BM-5g/ml after 6 and 24 hours of exposure. Interestingly, 2703 genes were significantly differentially expressed in HMDM upon exposure to 10M-BM-5g/ml ZnO nanoparticles, while in MDDCs only 12 genes were affected. In Jurkat cells, 980 genes were differentially expressed. It is noteworthy that the gene expression of metallothioneins was upregulated in all the three cell types. In addition to the common ZnO-inducible changes, a notable proportion of the genes were regulated in a cell type-specific manner. Using a panel of ZnO nanoparticles, we obtained an additional support that the cellular response to ZnO nanoparticles is caused by particle dissolution. Gene ontology analysis revealed that the top biological processes disturbed in HMDM and Jurkat cells were regulating cell death and growth. In addition, genes controlling immune system development were affected. Bioinformatics assessment showed that the top human disease category associated with ZnO-responsive genes in both HMDM and Jurkat cells was cancer. Overall, the study revealed novel genes and pathways for mediating ZnO nanoparticle-induced toxicity and demonstrated the value of assessing nanoparticle responses through combined transcriptomics and bioinformatics approach. Altogether 90 samples were analyzed originating from three biological replicates of HMDM, MDDC or Jurkat cells containg untreated control cells, ZnO or TiO2 treated cells with doses 1M-BM-5g/ml and 10M-BM-5g/ml. The sample timepoints were 6 hours and 24 hours.

Dataset Information

Expression data from mouse liver tissue from SKH:QS mice treated with commercially available sunscreens containing ZnO or TiO2 nanoparticles, or no nanoparticles

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure