Inter-laboratory comparison of pulmonary lesions induced by intratracheal instillation of NiO nanoparticle in rats: Histopathological examination results

Senoh, Hideki; Kano, Hirokazu; Suzuki, Michitaka; Fukushima, Shoji; Oshima, Yutaka; Kobayashi, Toshio; Morimoto, Yasuo; Izumi, Hiroto; Ota, Yasufumi; Takehara, Hiroshi; Numano, Takamasa; Kawabe, Mayumi; Gamo, Masashi; Takeshita, Jun-ichi

doi:10.1002/1348-9585.12117

Cited by 11 publications

(12 citation statements)

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“…Other studies reported that NiO NPs induced the histopathological changes in rats 10,11 and Ogami et al proved that NiO NPs increased collagen production in the rat lung tissues. 12 In addition, our previous studies confirmed that NiO NPs caused subchronic toxicity via inflammation and oxidative stress in rats.…”

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confidence: 94%

LncRNA MEG3 mediates nickel oxide nanoparticles‐induced pulmonary fibrosis via suppressing TGF‐β1 expression and epithelial‐mesenchymal transition process

Zhan

Chang

Wang

et al. 2021

Environmental Toxicology

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Nickel oxide nanoparticles (NiO NPs) causes pulmonary fibrosis via activating transforming growth factor-β1 (TGF-β1) in rats, but its upstream regulatory mechanisms are unknown. This study aimed to explore the role of long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) in NiO NPs-induced collagen deposition. Male Wistar rats were intratracheally instilled with NiO NPs (0.015, 0.06, and 0.24 mg/kg b.w.) twice a week for 9 weeks. Human lung adenocarcinoma epithelial cells (A549 cells) were cultured with NiO NPs (25, 50, and 100 μg/ml) to establish collagen deposition model. We discovered that NiO NPs-induced rat pulmonary fibrosis was accompanied by the epithelial-mesenchymal transition (EMT) occurrence and MEG3 down-regulation in rat lung tissues. In cell collagen deposition model, NiO NPs also evoked EMT and decreased MEG3 expression in a dose-dependent manner in A549 cells. By overexpressing MEG3 in A549 cells, we found that MEG3 inhibited the level of TGF-β1, EMT process and collagen formation. Moreover, our data showed that SB431542 (TGF-β1 inhibitor) had an inhibitory effect on NiO NPs-induced EMT and collagen formation. Our results indicated that MEG3 inhibited NiO NPs-induced collagen deposition by regulating TGF-β1-mediated EMT process, which may provide some clues for insighting into the mechanisms of NiO NPs-induced pulmonary fibrosis.

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confidence: 94%

LncRNA MEG3 mediates nickel oxide nanoparticles‐induced pulmonary fibrosis via suppressing TGF‐β1 expression and epithelial‐mesenchymal transition process

Zhan

Chang

Wang

et al. 2021

Environmental Toxicology

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“…It has been reported, for example, that asbestos and crystalline silica, which have high pulmonary toxicity, cause sustained inflammation in the lungs, leading to irreversible fibrosis, lung cancer and mesothelioma [ 11 , 12 ]. Thus, sustained inflammation is considered to be an important process in the induction of chronic and irreversible lesions of the lung [ 6 , 7 , 8 , 9 , 10 , 13 ]. MWCNTs, which are carcinogenic, have shown sustained inflammation in the lung following inhalation and intratracheal instillation [ 14 , 15 , 16 , 17 ].…”

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confidence: 99%

Predictive Biomarkers for the Ranking of Pulmonary Toxicity of Nanomaterials

et al. 2020

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We analyzed the mRNA expression of chemokines in rat lungs following intratracheal instillation of nanomaterials in order to find useful predictive markers of the pulmonary toxicity of nanomaterials. Nickel oxide (NiO) and cerium dioxide (CeO2) as nanomaterials with high pulmonary toxicity, and titanium dioxide (TiO2) and zinc oxide (ZnO) as nanomaterials with low pulmonary toxicity, were administered into rat lungs (0.8 or 4 mg/kg BW). C-X-C motif chemokine 5 (CXCL5), C-C motif chemokine 2 (CCL2), C-C motif chemokine 7 (CCL7), C-X-C motif chemokine 10 (CXCL10), and C-X-C motif chemokine 11 (CXCL11) were selected using cDNA microarray analysis at one month after instillation of NiO in the high dose group. The mRNA expression of these five genes were evaluated while using real-time quantitative polymerase chain reaction (RT-qPCR) from three days to six months after intratracheal instillation. The receiver operating characteristic (ROC) results showed a considerable relationship between the pulmonary toxicity ranking of nanomaterials and the expression of CXCL5, CCL2, and CCL7 at one week and one month. The expression levels of these three genes also moderately or strongly correlated with inflammation in the lung tissues. Three chemokine genes can be useful as predictive biomarkers for the ranking of the pulmonary toxicity of nanomaterials.

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“…Intratracheal instillation is a useful delivery method that requires only a small amount of test material and simple experimental equipment; it is therefore cost effective 4 , 5 , 6 . We have investigated the effects of various study conditions 7 and established a standardized test procedure for obtaining reliable results 8 , 9 . Accordingly, we have performed intratracheal instillation studies in rats to evaluate the comparative toxicities of several types of nano-sized titanium dioxide 10 , 11 , 12 and silicon dioxide materials (Kobayashi et al., in submission).…”

Section: Introductionmentioning

confidence: 99%

Time-course comparison of pulmonary inflammation induced by intratracheal instillation of four different nickel oxide nanoparticles in male Fischer rats

et al. 2021

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Occupational exposure to nickel oxide (NiO) is an important cause of respiratory tract cancer. Toxicity is known to be associated with the dissociated component, i.e. nickel (II) ions. To address the relationship between physicochemical properties, including solubility in artificial lysosomal fluid, of NiO and time-course changes in the pulmonary response, we conducted an intratracheal instillation study in male Fischer rats using four different well-characterized NiO products, US3352 (NiO A), NovaWireNi01 (NiO B), I small particle (NiO C), and 637130 (NiO D). The NiOs were suspended in purified water and instilled once intratracheally into male F344 rats (12 weeks old) at 0 (vehicle control), 0.67, 2, and 6 mg/kg body weight. The animals were euthanized on days 3, 28, or 91 after instillation, and blood analysis, bronchoalveolar lavage fluid (BALF) testing, and histopathological examination were performed. The most soluble product, NiO B, caused the most severe systemic toxicity, leading to a high mortality rate, but the response was transient and surviving animals recovered. The second-most-soluble material, NiO D, and the third, NiO A, caused evident pulmonary inflammation, and the responses persisted for at least 91 days with collagen proliferation. In contrast, NiO C induced barely detectable inflammation in the BALF examination, and no marked changes were noted on histopathology. These results indicate that the early phase toxic potential of NiO products, but not the persistence of pulmonary inflammation, is associated with their solubility.

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Inter-laboratory comparison of pulmonary lesions induced by intratracheal instillation of NiO nanoparticle in rats: Histopathological examination results

Abstract: This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

Cited by 11 publications

References 13 publications

LncRNA MEG3 mediates nickel oxide nanoparticles‐induced pulmonary fibrosis via suppressing TGF‐β1 expression and epithelial‐mesenchymal transition process

LncRNA MEG3 mediates nickel oxide nanoparticles‐induced pulmonary fibrosis via suppressing TGF‐β1 expression and epithelial‐mesenchymal transition process

Predictive Biomarkers for the Ranking of Pulmonary Toxicity of Nanomaterials

Time-course comparison of pulmonary inflammation induced by intratracheal instillation of four different nickel oxide nanoparticles in male Fischer rats

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