The molecular mechanism of Suguhiratake-acute encephalopathy;

2014 Fiscal Year Final Research Report

• Project/Area Number: 24248021
• Research Category: Grant-in-Aid for Scientific Research (A)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Bioproduction chemistry/Bioorganic chemistry
• Research Institution: Shizuoka University
• Principal Investigator: KAWAGISHI Hirokazu 静岡大学, グリーン科学技術研究所, 教授 (70183283)
• Co-Investigator(Kenkyū-buntansha): KAN Toshiyuki 静岡県立大学, 薬学部, 教授 (10221904) ; NAGAI Kaoru 山梨大学, 総合研究部, 准教授 (20340953) ; HIRAI Hirofumi 静岡大学, 農学研究科, 教授 (70322138) ; MORITA Tatsuya 静岡大学, 農学研究科, 教授 (90332692)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: キノコ / スギヒラタケ / 急性脳症 / pleurocybellaziridine

Outline of Final Research Achievements

We have a hypothesis of the molecular mechanism of Suguhiratake-acute encephalopathy; the complex between two macromolecules, a lectin (PPL) and B3, destroyed blood brain barrier (BBB), then a low-molecular-weight toxin, pleurocybellaziridine (PA) attacked the brain and caused the unique lesion. To confirm the hypothesis, we obtained the following results.
1) PA was stable when it coexisted with PPL and B3. 2) PA showed toxicity against oligodendrocyte. 3) Genome database of Suguhiratake was established. 4) Expression systems of recombinant PPL and B3 were successfully constructed. 5) The complex of rB3 and rPPL exhibited proteinase activity and destroyed BBB.

Free Research Field

天然物化学