Project description:The nematode C. elegans was exposed to TiO2 nanoparticles (NPs) to evaluate the ecotoxicity of TiO2 nanoparticles. We used the DNA microarray method to understand changes in gene expression after the exposure to TIO2 NPs. We identified various genes involved in metal detoxification as well as in regulating worm development.
Project description:ZnO nanoparticles can elicit a range of cytotoxic responses in different cells in vitro that may reflect either Zn2+ dissolution or nanoparticle-specific effects. Coating the ZnO nanoparticles may mitigate their cytotoxicity. We aimed to capture whole genome transcriptional profiles (up and down regulated) at time-points associated with distinct cytotoxic responses in cells treated with two types of uncoated (Nanosun, Z-COTE) or two types of coated (HP1, MAX) ZnO nanoparticles, compared to untreated cells. hONS cells were incubated with 25ug/ml ZnO nanoparticles (uncoated: Nanosun and Z-COTE; coated: MAX, HP1) for 2h and 6h and their expression profiles were compared to time-matched untreated cells.
Project description: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.
Project description:ZnO nanoparticles can elicit a range of cytotoxic responses in different cells in vitro that may reflect either Zn2+ dissolution or nanoparticle-specific effects. Coating the ZnO nanoparticles may mitigate their cytotoxicity. We aimed to capture whole genome transcriptional profiles (up and down regulated) at time-points associated with distinct cytotoxic responses in cells treated with two types of uncoated (Nanosun, Z-COTE) or two types of coated (HP1, MAX) ZnO nanoparticles, compared to untreated cells.
Project description: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.
Project description:ZnO nanoparticles can elicit a range of perturbed cell responses in vitro. The liver is a target for ZnO nanoparticle-, or Zn2+ released from ZnO nanoparticles-induced accumulation and/or impact in vitro and in vivo. The response of human hepatic stellate cells to ZnO nanoparticles has not yet been assessed. We aimed to determine whether the presence of surface coatings could protect human hepatic stellate cells from ZnO nanoparticle-induced cytotoxicity. Primary human hepatic stellate cells were treated with one of two types of uncoated ZnO nanoparticles (Z-COTE or Nanosun), two types of coated ZnO nanoparticles (HP1, MAX), a mass equivalent of ZnSO4, or were left untreated. After 24 h, RNA was isolated and processed for whole genome transcriptional profiling, comparing the expresson profiles of treated cells to the untreated controls. Each treatment was prepared in duplicate.
Project description:Here, we show that systems biology approaches can uncover mechanisms underlying cellular responses to nanomaterials. Using RNA Seq, we found that cationic nanoparticles are capable of triggering down-regulation of cell cycle-related genes in primary human bronchial epithelial cells at doses that do not elicit acute cytotoxicity. Bioinformatics analyses implicated NF-kappaB as a putative transcriptional regulator and functional assays confirmed that cationic nanoparticles caused NF-kappaB-dependent cell cycle arrest. Our study demonstrates the feasibility of applying systems biology tools to assess cellular responses to nanomaterials, not least at low doses.