1987 Fiscal Year Final Research Report Summary
Analysis of Brain Fatty Acid Metabolism and its Abnormality by Application of Monoclonal Antibody
| Project/Area Number |
60480143
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Nedical College of Oita |
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Principal Investigator |
TAKESHITA Masazumi Medical College of Oita, School of Medicine; Professor, 医学部, 教授 (50019551)
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| Co-Investigator(Kenkyū-buntansha) |
TAMURA Minoru Medical College of Oita, School of Medicine; Instructor, 医学部, 助手 (00128349)
YOSHIDA Satoshi Medical College of oita, School of Medicine; Assistant Professor, 医学部, 助教授 (50158440)
YUBISUI Toshitsugu Medical College of oita, School of Medicine; Assistant Professor, 医学部, 助教授 (00019564)
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| Project Period (FY) |
1985 – 1987
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| Keywords | Fatty acid elogation / Very-long-chain fatty acid elongation / Monoclonal antibody Arachidyl-CoA / Arachidonoyl-CoA / NADH-cytochrome b_5 reductase / Redio-liquid chromatography / ラジオ液体クロマトグラフィー / 副腎白質ジストロフィー症 |
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| Research Abstract |
In the present project, weinvestigated reaction systems of long- and very- long-chaine fatty acid elongation in detail. We prepared monoclonal antibodies for the enzymes and cytochromes involved in the elongation system, and investigated their application of the analysis of fatty acid metabolise and its abnormality in brain. The major results obtained are:
1) We decided the cDNA nucleotide sequence of NADH-cytochrome b_5 reductase which was involved in fatty acid elongation. We obtained monoclonal antibody possessing high titer for the reductase.
2) Computer simulation analysis revealed that the existence of wto parallel pathways in the very-long-chain fatty acid elongation in brain microsomes.
3) At least two separate condensing snzymes were involved in the elongation depending on the chain length of fatty acids.
4) In the elongation of arachidoyl-CoA and arachidonoyl-CoA condensation reaction waw evidenced to be rate limiting, and stereospecific S-sydrogen from NADPH was transfered in the reduction step.
5) We found an elongation condition to produce 26:0 and 26:1, which have been produced specifically in adrenoleukodystrophy patients. These results will give an approch for the cause and process of the demyelinationg disease.
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