1997 Fiscal Year Final Research Report Summary
Biological activity and biosynthetic mechanism of an emetic toxin produced by Bacillus cereus
| Project/Area Number |
08457086
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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 |
Bacteriology (including Mycology)
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| Research Institution | Nagoya University |
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Principal Investigator |
OHTA Michio School of Medicine Prof., 医学部, 教授 (20111841)
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| Co-Investigator(Kenkyū-buntansha) |
HORII Toshinobu School of Medicine Assistant Prof., 医学部, 助手 (80283430)
SHIBAYAMA Keigo School of Medicine Assistant Prof., 医学部, 助手 (50283437)
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| Project Period (FY) |
1996 – 1997
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| Keywords | cereulide / Bacillus cereus / foodborne illness / toxin / ionophore / liver failure / apotosis / mitochondria |
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| Research Abstract |
Cereulide is the causative toxin of the emetic type foodborne illness caused by Bacillus cereus. Our previous studies exhibited that it is a cyclic depsipeptide and a potassium ionophore and that it induces mitochondrial swelling in cultured HEp-2 cells. This toxin was associated with fulminant liver failure in a human case. Chemically synthesized cereulide had the same emetic effect as purified cereulide. BALB/c mice were i.p. injected with various dosed of synthetic or purified cereulide and the development of histopathological changes as well as physiological effects were examined. Hepatocytes showed the abnormality of the mitochondria such as swelling and loss of cristae. Dose-dependent increase of small fatty droplets in the degenerated hepatocytes was also observed. These microsteatotic hepatocytes were distributed in the pericentral area and spread to the intermediate and periportal areas. In the cases of lethal doses, massive degeneration of hepatocytes was prominent. These fatal lesions included massive microsteatosis and apotosis of hepatocytes. Other organs of these mice had no apparent specific pathological changes.
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