| Project/Area Number |
02807061
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Hygiene
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| Research Institution | National Institute for Environmental Studies. |
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Principal Investigator |
SAGAI Masaru Nat'l. Instit. Environ. Studies, Head researcher., 地域環境研究グループ・大気影響評価チーム, 総合研究官 (80124345)
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| Co-Investigator(Kenkyū-buntansha) |
OKADA Tomoko Nat'l Instit. Techni. Chemistry, Junior researcher., 化学技術研・生体機能化学部, 研究員
ICHINOSE Takamichi Nat'l. Instit. Environ. Studies Senior researcher., 地域環境研究グループ・大気影響評価チーム, 主任研究員 (50124334)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1991: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1990: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | Diesel exhaust particles / Supexid / Superoxide disumutase (SOD) / Hydroxyl radical / Endothelial cells / Active oxygens / Lipid peroxidation / Chronic obstructive pulmonary diseases / ス-パ-オキシド(O_2) / 肺胞マクロファ-ジ / 貪食能 / DNA鎖切断 / 肺水腫 |
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| Research Abstract |
Recently, air pollutants in big cities are very heavy and their effects on human health are serious. The main pollutants originate from diesel exhausts. Therefore, it is considered that diesel exhaust particles (DEP) may be causal compounds of lung cancers and chronic obstructive pulmonary diseases. On the other hand, the deleterious effects of oxygen radicals in the pathogenesis of chronic pulmonary diseases have been noticed. Here, as a part to make clear the pathogenesis of pulmonary diseases caused by DEP, it was examined whether pulmonary injury by DEP was due to oxygen radicals.
We found that DEP produced O^-_ and ・OH in vitro without any chemical or biochemical activating systems. Main chemical components of O^-_ generation were present in organic solvent extracted-fraction, because DEP washed with methanol lost the production-ability of O^-_ and ・OH. These oxygen radicals were identified by ESR measurement. DEP instillted intratracheally to mouse caused high mortality at low dose, although reethanol washed DEP exhibited no toxicity, at all. The cause of death was due to edema by epithelial cell damage. Marked species differences in mice on susceptibility to DEP were observed. The susceptibility was related to the ratio between the activity of antioxidative protective enzymes such as SOD and GPx in lungs caused by DEP and the control of activity. On the other hand, the mortality was protected markedly by intravenous injection or intratracheal instillation of SOD prior to DEP administration. DEP also caused inflammatory changes with infiltration of neutrophils and macrophages in the lungs.
Present results suggest that main parts of DEP toxicity is due to oxygen radicals such as O^-_ and ・OH and that the oxygen radicals generated from DEP cause inflammation, which is able to cause chronic pulmonary diseases.
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