| Project/Area Number |
10670356
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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 |
Public health/Health science
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| Research Institution | Kumamoto University |
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Principal Investigator |
NAGANO Megumi Kumamoto University, School of Medicine, Public Health, Lecturer, 医学部, 講師 (10136723)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Hideyuki Kumamoto University, School of Medicine, Pharmacology, Lecturer, 医学部, 講師 (60191433)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2000: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1999: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1998: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | 2,5-hexanedione / acrylamide / allyl chloride / neurotoxicity / neurofilament proteins / phosphorylation / calpain / 2,5-ヘキサンジオン / ニューロフィラメント / 2.5イキサンジオン / 二硫化炭素 |
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| Research Abstract |
Our purpose of the present studies was to elucidate the mechanism(s) of neulofilamentous axonopathy produced by 2,5-hexanedione (HD), acrylamide (AM) or allyl chloride (AC) treatments in vivo and in vitro using the NF-rich fraction from the spinal cords of Donryu rats.
The new results obtained were as follows; 1) Significantly high amount (p< 0.0 l) of cross-linked NF proteins were observed in NF-fraction from HD-intoxicated animals and not in that from AM or AC-intoxiated animals, 2) the cross-linked NF proteins contained significantly (p< 0.05) higher amount of dephosphorylated NFs compared to its original NF-H and/or NF-M bands, 3) the time-course study of the reactions ofphosphorylated or dephosphorylated NF proteins with HD in vitro revealed that the appearance of cross-linked NF proteins were much more after the reaction of dephosphorylated NF with HD, and 4) the degradations of NF-H subunit protein by calpain-contained supernatant fraction obtained from the spinal cords ofAM-intoxicated rats were significantly (p< 0.05) retarded when compared to those from control rats.
The whole pathogenesis of neurofilamentous axonopathies was not fully clarified. We further need to study not only the effects of these chemicals on NF proteins but also on the other cytoskeletal proteins such as tubulin, microtubule-associated proteins and tau-protein
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