Expression of Heme Oxygenase-1 in the Lungs of Rats Exposed to Crocidolite Asbestos

Nagatomo, Hiroko; Morimoto, Yasuo; Oyabu, Takako; Hirohashi, Masami; Ogami, Akira; Kuroda, Kaori; Higashi, Toshiaki; Tanaka, Isamu

doi:10.1080/08958370590922580

Cited by 20 publications

(16 citation statements)

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“…Increased HO-1 expression has also been reported in human interstitial pneumonia (UIP) 5) and cystic fibrosis (CF) 6) . Increased HO-1 expression has also been found in our study of a lung injury model in which rats were exposed to asbestos 7,8) and crystalline silica 9) ; therefore, HO-1 is thought to be related to lung injury caused by dust.…”

supporting

confidence: 67%

“…Therefore, the expression of protein (concentration of HO-1 protein / protein exactly) was increased from the acute phase as an acute inflammatory reaction. We have also reported that more alveolar macrophages were stained for HO-1 in rats exposed to crocidolite, chrysotile and crystalline silica compared with the control groups [7][8][9] . Maestrelli et al reported that HO-1-positive macrophages were increased in smokers with chronic obstructive pulmonary disease (COPD) as compared with nonsmoking subjects in an immunohistochemistry study of human lung surgical specimens 13) .…”

Section: Discussionmentioning

confidence: 58%

“…These findings reveal that asbestos and crystalline silica, which are hazardous to the lung, significantly and persistently increased the HO-1 protein expression. On the other hand, less hazardous titanium dioxide (TiO 2 ) did not induce an increased HO-1 expression [7][8][9] . The protein expression pattern of the HO-1 gene in the present study was persistent though mild in the chronic phase.…”

Section: Discussionmentioning

confidence: 97%

“…Nagatomo et al examined HO-1 gene expression in animal lung tissue from 3 days to 3 mo after intratracheal instillation of crocidolite and reported a persistent increase in HO-1 gene protein expression 7) . Similar intratracheal instillations of crystalline silica, fine silica and chrysotile showed increased HO-1 gene protein expression in both the acute and chronic phases 8,9) .…”

Section: Discussionmentioning

confidence: 99%

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Expression of Heme Oxygenase‐1 in the Lungs of Rats Exposed to Potassium Octatitanate Whiskers

Obata

Morimoto

Hirohashi

et al. 2011

Journal of Occupational Health

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Expression of Heme Oxygenase-1 in the Lungs of Rats Exposed to Potassium Octatitanate Whiskers: Yasuko Obata, et al. Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Japan-Objectives: Oxidative stress is thought to be the pathogenesis of pulmonary fibrosis induced by asbestos, and heme oxygenase-1 (HO-1) protects lung tissue against oxidative stress. We hypothesized that HO-1 is also associated with oxidative lung injury caused by exposure to potassium octatitanate whiskers (PT1), which is one of the asbestos substitutes. Methods: Male Wistar rats were administered 1 mg or 2 mg PT1 suspended in saline by a single intratracheal instillation and were sacrificed after recovery for 3 days, 1 wk, 1 mo, 3 mo or 6 mo. Gene expression of HO-1 protein and mRNA and immunostaining were investigated in rat lungs. Results: HO-1 protein expression was increased from 3 days to 1 mo and at 6 mo in the 1 or 2 mg PT1-exposed groups, and the gene expression of HO-1 mRNA was also increased at 3 days and from 1 mo to 6 mo. HO-1-positive cells were mainly found in the alveolar macrophages and the bronchial epithelial cells in immunostaining. Conclusions: These findings suggest that HO-1 is involved in lung damage caused by PT1. (J Occup Health 2011; 53: 267-273)

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confidence: 67%

Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

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Expression of Heme Oxygenase‐1 in the Lungs of Rats Exposed to Potassium Octatitanate Whiskers

Obata

Morimoto

Hirohashi

et al. 2011

Journal of Occupational Health

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“…Hemoglobin metabolism is mediated by heme oxygenase-1, which is upregulated when animals or cells are treated with asbestos. (68,69) Therefore, this Refer to Table S1 for details.…”

Section: Discussionmentioning

confidence: 99%

Asbestos surface provides a niche for oxidative modification

et al. 2011

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Asbestos is a potent carcinogen associated with increased risks of malignant mesothelioma and lung cancer in humans. Although the mechanism of carcinogenesis remains elusive, the physicochemical characteristics of asbestos play a role in the progression of asbestos-induced diseases. Among these characteristics, a high capacity to adsorb and accommodate biomolecules on its abundant surface area has been linked to cellular and genetic toxicity. Several previous studies identified asbestos-interacting proteins. Here, with the use of matrix-assisted laser desorption ionization-time of flight mass spectrometry, we systematically identified proteins from various lysates that adsorbed to the surface of commercially used asbestos and classified them into the following groups: chromatin ⁄ nucleotide ⁄ RNA-binding proteins, ribosomal proteins, cytoprotective proteins, cytoskeleton-associated proteins, histones and hemoglobin. The surfaces of crocidolite and amosite, two iron-rich types of asbestos, caused more protein scissions and oxidative modifications than that of chrysotile by in situ-generated 4-hydroxy-2-nonenal. In contrast, we confirmed the intense hemolytic activity of chrysotile and found that hemoglobin attached to chrysotile, but not silica, can work as a catalyst to induce oxidative DNA damage. This process generates 8-hydroxy-2¢-deoxyguanosine and thus corroborates the involvement of iron in the carcinogenicity of chrysotile. This evidence demonstrates that all three types of asbestos adsorb DNA and specific proteins, providing a niche for oxidative modification via catalytic iron. Therefore, considering the affinity of asbestos for histones ⁄ DNA and the internalization of asbestos into mesothelial cells, our results suggest a novel hypothetical mechanism causing genetic alterations during asbestos-induced carcinogenesis. (Cancer Sci 2011; 102: 2118-2125 A sbestos is a natural fibrous mineral that was heavily used in industry during the past century because of its durability, heat resistance and low cost. However, it has become clear that respiratory exposure to asbestos fibers, especially crocidolite and amosite, which have high biopersistence and contain abundant iron, is associated with high risks of developing malignant mesothelioma and lung cancer.(1-3) Many countries anticipate increased numbers of mesothelioma patients in the coming decades because there is an extremely long incubation period (30-40 years) for this fatal disease following asbestos exposure. (4) The molecular mechanism of asbestos-induced carcinogenesis remains elusive, (5) but both mesothelial cell injury and persistent macrophage activation are thought to be essential, if not sufficient, for mesotheliomagenesis.(6) These two events interact in vivo, leading to genetic mutations, chromosomal aberrations and aneuploidy in mesothelial cells. At least four major hypotheses related to the underlying mechanisms have been proposed. (6,7) First, the free radical theory postulates that DNA is injured by reactive oxygen species generated th...

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Apoptotic, inflammatory, and fibrogenic effects of two different types of multi-walled carbon nanotubes in mouse lung

et al. 2014

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There is increasing concern about the toxicity of inhaled multi-walled carbon nanotubes (MWCNTs). Pulmonary macrophages represent the primary cell type involved in the clearance of inhaled particulate materials, and induction of apoptosis in these cells has been considered to contribute to the development of lung fibrosis. We have investigated the apoptotic, inflammogenic, and fibrogenic potential of two types of MWCNTs, characterised by a contrasting average tube length and entanglement/agglomeration. Both nanotube types triggered H2O2 formation by RAW 264.7 macrophages, but in vitro toxicity was exclusively seen with the longer MWCNT. Both types of nanotubes caused granuloma in the mouse lungs. However, the long MWCNT induced a more pronounced pro-fibrotic (mRNA expression of matrix metalloproteinase-8 and tissue inhibitor of metalloproteinase-1) and inflammatory (serum level of monocyte chemotactic protein-1) response. Masson trichrome staining also revealed epithelial cell hyperplasia for this type of MWCNT. Enhanced apoptosis was detected by cleaved caspase 3 immunohistochemistry in lungs of mice treated with the long and rigid MWCNT and, to a lesser extent, with the shorter, highly agglomerated MWCNT. However, staining was merely localised to granulomatous foci, and neither of the MWCNTs induced apoptosis in vitro, evaluated by caspase 3/7 activity in RAW 264.7 cells. In addition, our study reveals that the inflammatory and pro-fibrotic effects of MWCNTs in the mouse lung can vary considerably depending on their composition. The in vitro analysis of macrophage apoptosis appears to be a poor predictor of their pulmonary hazard.

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Expression of Heme Oxygenase-1 in the Lungs of Rats Exposed to Crocidolite Asbestos

Cited by 20 publications

References 16 publications

Expression of Heme Oxygenase‐1 in the Lungs of Rats Exposed to Potassium Octatitanate Whiskers

Expression of Heme Oxygenase‐1 in the Lungs of Rats Exposed to Potassium Octatitanate Whiskers

Asbestos surface provides a niche for oxidative modification

Apoptotic, inflammatory, and fibrogenic effects of two different types of multi-walled carbon nanotubes in mouse lung

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