Expression of Heme Oxygenase‐1 in the Lungs of Rats Exposed to Crystalline Silica

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

doi:10.1539/joh.48.124

Cited by 18 publications

(14 citation statements)

References 21 publications

(23 reference statements)

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“…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: 57%

“…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) . These findings reveal that asbestos and crystalline silica, which are hazardous to the lung, significantly and persistently increased the HO-1 protein expression.…”

Section: Discussionmentioning

confidence: 82%

“…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: 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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Section: Discussionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 82%

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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“…Our previous study using crystalline silica showed that even if the particles are of the same chemical composition, their biological effects vary depending on their particle size 4) . Hazard assessment of newly-generated respirable particles must therefore be conducted for such differences and various biomarker studies are currently being implemented to objectively and quantitatively assess the hazards of such substances [5][6][7][8][9][10][11][12][13][14] .…”

Section: Background and Objectivesmentioning

confidence: 99%

Analysis of Bronchoalveolar Lavage Fluid Adhering to Lung Surfactant

Kadoya¹,

Ogami²,

Morimoto³

et al. 2012

Ind Health

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Nickel oxide with two different particle sizes, micron size (NiO) and submicron size (nNiOm), as well as crystalline silica as a positive control and titanium dioxide as a negative control, were intratracheally instilled in rats and the phospholipid concentration and the protein concentration and surface tension of bronchoalveolar lavage fluid (BALF), which are used in surfactant assessment, were measured to see if they could be effective biomarkers in toxicity assessment. The results showed that the NiO instilled group showed no significant difference compared to the control group throughout the observation period. In contrast, a significant difference was found in the nNiOm instilled group compared to the control group throughout the observation period. Moreover, a significant difference was found in the crystalline silica instilled group for each measurement compared to the control group while for the titanium dioxide group, almost no significant difference was found. These results indicate that submicronsized particles of nickel oxide with smaller median diameters potentially have a stronger biological effect than micron size particles. They also indicate that screening can be done by measuring the phospholipid concentration and the protein concentration and surface tension of BALF.

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“…Simultaneously, anti-oxidative responses such as production of glutathione and expression of heme oxygenase-1 (HO-1) are activated 17,18) . Inhalation of asbestos and crystalline silica induce severe oxidative stress and subsequent expression of HO-1 19,20) . Detection of the level of oxidative stress is an important factor in forecasting a disease.…”

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confidence: 99%

Evaluation of Acute Oxidative Stress Induced by NiO Nanoparticles In Vivo and In Vitro

Horie

Fukui

Nishio

et al. 2011

Journal of Occupational Health

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103

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Evaluation of Acute Oxidative Stress Induced by NiO Nanoparticles In Vivo and In Vitro:Masanori Horie, et al. Health Research Institute -Objectives: Nickel oxide (NiO) is an important industrial material, and it is also a harmful agent. The toxicity of NiO is size-related: nanoparticles are more toxic than fine-particles. The toxic mechanism induced by NiO nanoparticles remains unexplained, and the relationship between in vitro and in vivo NiO toxicity results is unclear. In the present study, we focused on the oxidative stress caused by NiO nanoparticles by examining and comparing in vitro and in vivo acute responses induced by NiO nanoparticles. Methods: Cellular responses induced by black NiO nanoparticles with a primary particle size of 20 nm, were examined in human lung carcinoma A549 cells. In vivo responses were examined by instillation of NiO nanoparticles into rat trachea. Bronchoalveolar lavage fluid (BALF) was collected after intratracheal instillation at different time points, and concentrations of lipid peroxide heme oxygenase-1 (HO-1), surfactant protein-D (SP-D) and lactate dehydrogenase (LDH) in BALF were measured. Results: The levels of intracellular reactive oxygen species and lipid peroxidation in A549 cells increased with increasing exposure to NiO nanoparticles, and increases in gene expressions of HO-1 and SP-D were observed in A549 cells. The lipid peroxide level in BALF significantly increased after 24 h instillation but decreased three days later. LDH leakage was also observed three days later. Conclusions: NiO nanoparticles induce oxidative stress-related lung injury. In vivo and in vitro oxidative stress was induced resulting in activation of antioxidant systems. Based on these responses, we conclude that the results of the in vivo and in vitro studies tend to correspond. (J Occup Health 2011; 53: 64-74)

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Expression of Heme Oxygenase‐1 in the Lungs of Rats Exposed to Crystalline Silica

Cited by 18 publications

References 21 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

Analysis of Bronchoalveolar Lavage Fluid Adhering to Lung Surfactant

Evaluation of Acute Oxidative Stress Induced by NiO Nanoparticles In Vivo and In Vitro

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