2005 Fiscal Year Final Research Report Summary
Examination of molecular biomarkers of lung injury induced by new inhaled materials
| Project/Area Number |
16590493
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hygiene
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
NAGATOMO Hiroko UOEH, Institute of Industrial and Ecological Sciences, Research Associate, 産業生態科学研究所, 助手 (10369077)
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| Co-Investigator(Kenkyū-buntansha) |
MORIMOTO Yasuo UOEH, IIES, Professor, 産業生態科学研究所, 教授 (30258628)
HIROHASHI Masami UOEH, IIES, Research Assistant, 産業生態科学研究所, 教務職員 (50389475)
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| Project Period (FY) |
2004 – 2005
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| Keywords | new inhaled materials / lung injury / oxidative stress / heme oxygenase-1 |
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| Research Abstract |
Male Wistar rats were administered crystalline silica, asbestos (crocidolite, chrysotile), newly inhaled materials (PT1 ; Potassium octatitanate whisker, SiCW ; silicon carbide whisker) or Titanium dioxide (TiO_2, negative control) by a single intratracheal instillation and were sacrificed at 3 days, 1 week, 1 month, 3 months and 6 months of recovery time. The HO-1 protein levels were unchanged at from 3 days to 6 months after the instillation of PT1,SiCW or TiO_2, which cause reversible inflammation in rat lung. However, exposure to crystalline silica, crocidolite or chtysotile, which cause irreversible inflammation in rat lung, significantly increased the HO-1 expression at from 3 days to 6 months.
HO-1 mRNA expression significantly increased after a single exposure to chrysotile. On the other hand, HO-1 mRNA expression decreased at 3 days and 1 month after the instillation of TiO_2.
In vitro, increased expression of HO-1 protein was found time and dose dependency after exposure to chrysotile. On the other hand, there were no HO-1 protein expression changes in the cells exposed to TiO_2 or newly inhaled materials
In summary, advancement of lung injury may be differentiated by the HO-1 expression in lung. Analysis of HO-1 expression may be helpful in detecting irreversible lung tissue injury, and therefore HO-1 can act as a biomarker of lung injury due to dust exposure.
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