| Project/Area Number |
16500526
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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 |
Eating habits, studies on eating habits
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| Research Institution | Mukogawa Women's University (2004, 2006)
Mukogawa Women's University Junior College Division (2005) |
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Principal Investigator |
DOI Hiroshi Mukogawa Women's University, School of Human Environmental Sciences, Professor, 生活環境学部, 教授 (50106267)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2006: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | oxidative stress / phosphatidylcholine hydroperoxide / membrane lipid / microtubules / tubulin / PC12細胞 / 細胞膜損傷 / 抗酸化系 / GTPase / 細胞膜 / 細胞分化 / 神経突起 / 細胞骨格 / 細胞生育 / 神経突起形成 |
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| Research Abstract |
Lipid peroxidation traditionally has been regarded as the major process causing damage to the brain by oxygen radicals and, subsequently, some forms of age-related deterioration. The brain, with its high oxygen consumption and abundance of polyunsaturated fatty acids, is at risk for oxidative damage. Although a great number of reports have associated lipid peroxidation with neurodegenerative diseases, the precise target of lipid peroxidation remains unclear. The aim of this study was to clarify the precise target of lipid hydroperoxides in neuronal cells. In this study, we showed the deleterious effect of phosphatidylcholine hydroperoxides (PCOOH) on PC 12 cells before and after differentiation into neuronal cells. Cell viability was significantly decreased in differentiated cells treated with PCOOH compared to undifferentiated cells treated in a similar way. PCOOH disrupted the formation of neurites and neuronal microtubules, which consist mainly of tubulin. Our results showed that differentiated cells were more vulnerable than undifferentiated cells to PCOOH and that PCOOH could attack microtubule-tubulin systems. This is the first study to clarify the effect on neuronal cells of PCOOH produced in the early stage of neurodegenerative disease and to elucidate the target of lipid hydroperoxide.
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