2004 Fiscal Year Final Research Report Summary
Risk assessment of sick house syndrome by chemical compounds
| Project/Area Number |
14370129
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Kansai Medical University |
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Principal Investigator |
MASAKI Ryuichi Kansai Medical University, Faculty of Medicine, Assistant Professor, 医学部, 講師 (70140283)
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| Co-Investigator(Kenkyū-buntansha) |
FUJISAWA Jun-ichi Kansai Medical University, Faculty of Medicine, Professor, 医学部, 教授 (40181341)
TAKETANI Shigeru Kyoto Institute of Technology, Department of Biotechnology, Professor, 繊維学部, 教授 (20121949)
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| Project Period (FY) |
2002 – 2004
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| Keywords | sick-house syndrome / stress marker / heme oxygenase-1 / formaldehyde / Reactive oxygen species / phthalate ester / GFP / Stress |
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| Research Abstract |
To investigate the responsibility of sick-house syndrome, the relationship of organic chemicals including phtalic acid ester and formaldehyde to the variations of stress markers was examined. First the determination of these compounds with house dust was established and we found that fluorescent light reduced those amounts. We next focused on a stress-inducible enzyme, heme oxygenase (HO)-1 which degrades heme into biliverdin, iron and CO, as a stress marker. The enzyme participates in adaptive and protective responses to oxidative stress and various inflammatory stimuli since most of the known HO-1 inducers stimulate the production of ROS or lead to a depletion of glutathione levels. We examined the regulation of HO-1 expression in culture cells under uninduced conditions. Observations by in situ hybridization and immunostaining showed that in cultured mouse fibroblast Balb/3T3 cells not subjected to treatment, 10-15% of cells highly expressed HO-1. The similar pattern of the expression of HO-1 was observed with BNL-CL2 and CHO cells. The marked expression of HO-1 was related to the activation of SAPK/JNK and to the expression of Cox-2. When the cells were treated with arachidonic acid, a precursor of prostaglandin, induction of HO-1 in the HO-1-expressing cells but not in the low-expressing cells occurred. This increase was abrogated by the treatment with the Cox inhibitor, indomethacin and dexamethasone. Neither prostaglandin H_2,E_2 nor F_<2a> induced HO-1 expression. These results suggest that some cells respond to the cellular stress and intermediates of prostaglandin biosynthesis may act as endogenous stressors to induce HO-1.
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[Journal Article] p38 MAPK mediates fibrogenic signal through Smad3 phosphorylation in rat myofibroblasts2003
Author(s)
Furukawa F, Matsuzaki K, Mori S, Tahashi Y, Yoshida K, Sugano Y, Yamagata H, Matsushita M, Seki T, Inagaki Y, Nishizawa M, Fijisawa J, Inoue K
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Journal Title
Hepatology 38
Pages: 879-889
Description
「研究成果報告書概要(和文)」より
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[Journal Article] p38 MAPK mediates fibrogenic signal through Smad3 phosphorylation in rat myofibroblasts.2003
Author(s)
Furukawa F, Matsuzaki K, Mori S, Tahashi Y, Yoshida K, Sugano Y, Yamagata H, Matsushita M, Seki T, Inagaki Y, Nishizawa M, Fujisawa J, Inoue K
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Journal Title
Hepatology 38
Pages: 879-889
Description
「研究成果報告書概要(欧文)」より
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