2005 Fiscal Year Final Research Report Summary
New evaluation system of cell damage caused by environmental chemicals that effect lifestyle diseases
| Project/Area Number |
15310033
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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 |
Risk sciences of radiation/Chemicals
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| Research Institution | University of Tsukuba |
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Principal Investigator |
ISHII Tetsuro University of Tsukuba, Majors of Medical Sciences, Graduate School of Comprehensive Human Sciences, Professor, 大学院・人間総合科学研究科, 教授 (20111370)
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| Co-Investigator(Kenkyū-buntansha) |
KUMAGAI Yoshito University of Tsukuba, Graduate School of Comprensive Human Science, Professor, 大学院・人間総合科学研究科, 教授 (00250100)
YANAGAWA Toru University of Tsukuba, Graduate School of Comprensive Human Science, Assistant Professor, 大学院・人間総合科学研究科, 講師 (10312852)
WARABI Eiji University of Tsukuba, Graduate School of Comprensive Human Science, Assistant Professor, 大学院・人間総合科学研究科, 講師 (70396612)
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| Project Period (FY) |
2003 – 2005
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| Keywords | Prx I / Fe-NTA / HO-1 / A170 / Nrf2 / CD36 / A549 / phenanthraquinone |
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| Research Abstract |
1.Cytotoxicity of phenanthraquinone contained in diesel exhaust particles
Phenanthraquinone showed strong toxicity to cultured human A549 cells derived from lung. Phenanthroline protected cells from toxicity of phenanthraquinone.
2.Cytotoxicity of arsenic compounds
Arsenic activates transcription factor Nrf2 and activate expression of genes such as HO-1,Prx I and A170, the protein accumulated as ubiquitin-conjugated form. Sulforaphane, Nrf2 activating natural compounds, had a beneficial effects against arsenic toxicity.
3.Analysis of model mice in lifestyle-related illnesses
We constructed Prx I-deficient transgenic mice. The mutant mice showed higher sensitivity of tissue oxidative damage to Fe-NTA. The mice showed lower capacity to remove nitroxyl radicals. We also constructed A170-deficient mice. These mice show overeating and obesity, causing insulin-resistance.
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