Similar pulmonary toxicity and gene expression changes after short-term inhalation exposure to surface-modified copper oxide nanoparticles
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PROVIDER: PRJNA666921 | ENA |
REPOSITORIES: ENA
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Project description:This study investigated the pulmonary toxicity of Copper oxide nanoparticles (CuO NPs) surface modified with polyethylenimine (PEI) or ascorbate (ASC), was investigated. Rats were exposed nose-only to a fixed exposure concentration of ASC or PEI coated CuO NPs for 5 consecutive days. On day 6 and day 27 post-exposure, pulmonary toxicity markers in bronchoalveolar lavage fluid (BALF) were analyzed and histopathological evaluation of the lungs was performed, along with microarray analyses on whole lung tissue samples.
2020-10-02 | GSE158900 | GEO
Project description:Copper oxide nanoparticles (CuO NPs) are considered for various technological and consumer applications, leading to growing concerns for potential human hazards resulting from inhalation. Recent studies have revealed a dose-dependent toxicity of CuO NPs in rats following short-term inhalation exposure. Here, we utilized transcriptomics approaches to further investigate the responses in rats exposed via inhalation for five consecutive days to two doses of CuO NPs, 3.3 (low dose, LD) and 13.2 (high dose, HD) mg/m3, with collection of lung tissues on days 6 (1 day post-exposure) and 28 (i.e., after a 22-day post-exposure recovery period). Histopathology confirmed an acute inflammatory response that was resolved during the post-exposure phase. Global gene expression analyses yielded about 1,000 differentially expressed genes in HD rats and 200 in LD on day 6, and less than 20 after the recovery period. Pathway analysis indicated cell proliferation/survival and inflammation as the main processes triggered by exposure and identified epithelial cell transforming protein 2 (Ect2) as a potential gene of interest implicated in cell proliferation. Indeed, ECT2 was upregulated in exposed lungs and was localized in the cytoplasm of alveolar epithelial cells in HD rats, in hyperplasic foci identified based on the Ki67 antigen, a marker of cell proliferation. Monocyte chemoattractant protein 1 (MCP-1, also known as CCL2), with an important role in the regulation of inflammatory processes and cell proliferation, was also upregulated and this was confirmed immunohistochemically. Finally, we could not find any evidence for aberrant DNA methylation of inflammation-associated genes in response to CuO NP exposure. In summary, the current findings suggest that airborne CuO NPs cause an acute response that translates into inflammation and cellular proliferation in bronchoalveolar epithelium, with upregulation of neoplasia-related factors even after a short-term exposure.
2018-09-01 | GSE86390 | GEO
Project description:Copper oxide nanoparticles treated C57 mice
| PRJNA1209058 | ENA
Project description:Copper oxide nanoparticles treated MH-S cells
| PRJNA1211049 | ENA
Project description:To identify the molecular impact of SPIO nanoparticle inhalation exposure on lung tissue. Transcriptional responses were measured by global microarray analysis of mouse lung. Male Balb/c mice were exposed to aerosolized SPIO nanoparticles using a nano-aerosol generation and inhalation system . Exposure was performed using two groups of 30 male Balb/c mices (60 total). One group of 30 was exposed to aerosolized SPIO nanopartic
2014-04-15 | E-GEOD-51417 | biostudies-arrayexpress
Project description:Inhalation and low-dose aspiration elicit highly similar pulmonary inflammation which was confirmed by activation of essentially similar biological pathways and even the same genes. Present results provide evidence that oropharyngeal aspiration is valid approach for hazard assessment of nanomaterials and proper alternative method for inhalation exposure.
2017-05-01 | GSE85711 | GEO
Project description:The C57BL/6J mice were randomly divided into three groups: control group (n=3), CuO NPs group (n=3), and CuO NPs + TTM group (n=3). A suspension of 2 mg/mL CuO NPs in 100 μl sterile saline was directly once administered by intratracheal instillation in CuO NPs treatment group. Mice in control group received 100 μl sterile saline. In the CuO NPs + TTM intervention group, 0.02 mg/mL TTM was added to the daily drinking water. All mice were sacrificed on day 7. Total RNA of the mouse lung tissues were extracted using tissue RNA isolation kit. All samples were sent to Majorbio Biotech (Shanghai, China) for transcriptome sequencing.
2025-01-13 | GSE286391 | GEO
Project description:This study proposes a molecular mechanism for lung epithelial A549 cell response to copper oxide nanoparticles (CuO-NPs) related to Cu ions released from CuO-NPs. Cells that survived exposure to CuO-NPs arrested the cell cycle as a result of the downregulation of proliferating cell nuclear antigen (PCNA), cell division control 2 (CDC2), cyclin B1 (CCNB1), target protein for Xklp2 (TPX2), and aurora kinase A (AURKA) and B (AURKB). Furthermore, cell death was avoided through the induced expression of nuclear receptors NR4A1 and NR4A3 and growth arrest and DNA damage-inducible 45 β and γ (GADD45B and GADD45G, respectively). The downregulation of CDC2, CCNB1, TPX2, AURKA, and AURKB, the expressions of which are involved in cell cycle arrest, was attributed to Cu ions released from CuO-NPs into medium. NR4A1 and NR4A3 expression was also induced by Cu ions released into the medium. The expression of GADD45B and GADD45G activated the p38 pathway that was involved in escape from cell death. The upregulation of GADD45B and GADD45G was not observed with Cu ions released into medium but was observed in cells exposed to CuO-NPs. However, because the expression of the genes was also induced by Cu ion concentrations higher than that released from CuO-NPs into the medium, the expression appeared to be triggered by Cu ions released from CuO-NPs taken up into cells. We infer that, for cells exposed to CuO-NPs, those able to make such a molecular response survived and those unable to do so eventually died. Two-condition experiment, CuO-NPs exposured vs. non-treated cells. Hybridization: 2 replicates. Scanning: 3 replicates (Gain changed).
2012-01-05 | E-GEOD-33278 | biostudies-arrayexpress
Project description:This study proposes a molecular mechanism for lung epithelial A549 cell response to copper oxide nanoparticles (CuO-NPs) related to Cu ions released from CuO-NPs. Cells that survived exposure to CuO-NPs arrested the cell cycle as a result of the downregulation of proliferating cell nuclear antigen (PCNA), cell division control 2 (CDC2), cyclin B1 (CCNB1), target protein for Xklp2 (TPX2), and aurora kinase A (AURKA) and B (AURKB). Furthermore, cell death was avoided through the induced expression of nuclear receptors NR4A1 and NR4A3 and growth arrest and DNA damage-inducible 45 β and γ (GADD45B and GADD45G, respectively). The downregulation of CDC2, CCNB1, TPX2, AURKA, and AURKB, the expressions of which are involved in cell cycle arrest, was attributed to Cu ions released from CuO-NPs into medium. NR4A1 and NR4A3 expression was also induced by Cu ions released into the medium. The expression of GADD45B and GADD45G activated the p38 pathway that was involved in escape from cell death. The upregulation of GADD45B and GADD45G was not observed with Cu ions released into medium but was observed in cells exposed to CuO-NPs. However, because the expression of the genes was also induced by Cu ion concentrations higher than that released from CuO-NPs into the medium, the expression appeared to be triggered by Cu ions released from CuO-NPs taken up into cells. We infer that, for cells exposed to CuO-NPs, those able to make such a molecular response survived and those unable to do so eventually died.
2012-01-05 | GSE33278 | GEO
Project description:BackgroundThis study aimed to compare the toxic effects of three different titanium dioxide nanoparticles encoded in the European nanomaterial repository as NM-103 (rutile, hydrophobic), NM-104 (rutile, hydrophilic), and NM-105 (anatase/rutile, hydrophilic), suggesting different toxic potentials after uptake in the lungs. Wistar rats were exposed by nose-only inhalation to aerosol concentrations of 3, 12 and 48 mg/m3 for 4 weeks. This dosing scheme should induce non, partial and complete lung overload. The 4-week inhalation period was followed by 3-, 45- and 94-day exposure-free periods. Investigations according to the OECD 412 guideline were performed. Additional examinations, such as transmission electron microscopy and image analysis of tissue slides and cytospots, were performed to reveal possible differences among the three particle types.ResultsBronchoalveolar lavage fluid from the groups exposed to low concentrations of NM-103 or NM-104 presented slight inflammation. In the mid- and high-exposure groups, this was also present for the NM-105 group, however, weaker than those of NM-103 and NM-104. Histologically, all three groups presented similar distributions of particles in the respiratory tract. Although marginal differences in the degree of some changes exist, no obvious differences in the degree or characteristics of the induced lesions were observable. In general, compared with the higher exposure groups, all the middle exposure groups presented a greater accumulation and aggregation of macrophages at the terminal bronchi. Using transmission electron microscopy, particles were detected mainly in intraalveolar macrophages, followed by type 1 pneumocytes in the low- and mid-concentration groups and intraalveolar free particles in the high-concentration groups. Compared with the other groups, the NM-103 group presented greater numbers of free particles in the alveoli and fewer in the macrophages. With image analysis, the movement of particles to the bronchus-associated lymphoid tissue and lymph nodes could be detected comparably for the three different particle types.ConclusionsThe no observed adverse effect concentration was 3 mg/m3 for all three different TiO2 particles. Despite minimal differences, a ranking mainly based on granulocyte influx into the lung was NM-104 > NM-103 > NM-105.
| S-EPMC11849269 | biostudies-literature