| Project/Area Number |
61560344
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
基礎獣医学
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| Research Institution | Faculty of Agriculture, Kagoshima University |
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Principal Investigator |
SHIMIZU Tsutomu Faculty of Agriculture, Kagoshima University, 農学部, 助教授 (50072921)
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| Co-Investigator(Kenkyū-buntansha) |
安田 宣紘 鹿児島大学, 農学部, 助手 (30041651)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1987: ¥100,000 (Direct Cost: ¥100,000)
Fiscal Year 1986: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | cycasin / cycad poisoning / goat / hepatotoxicity / spinal cord lesions / 脊髄病変 / 肝性脳症 |
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| Research Abstract |
Cycasin is a principal toxin contained in cycad plant and has potent hepatotoxicity and cacinogenicity. Naturally occurring cycad-poisoning in cattle is characterized by ataxia in hindquarters with demyelination and axonal degeneration in the spinal cord white matter, while cycad-poisoning in sheep is known to show marked hepatotoxicity and cerebral injury. No pathological study has been made on cycad-poisoned goats. In the previous study 2 goats chronically intoxicated with cycasin showed paretic signs in hindquarters. The goats had hepatic lesions and leukomyelopathy qualitatively similar to cycad-poisoning in cattle. To elucidate role of cycasin in cycad poisoning, 7 goats experimentally poisoned by ingestion of cycad leaves and 5 goats given various lethal doses of cycasin were compared pathologically.
Cycad poinsoning in goats was proved to show obvious hepatotoxicity comparable to that in sheep. Cycasin intoxicated goats presented severer hepatic lesions than those in the previous study by smaller dosages of the toxin, and failed to reproduce the leukomyelopathic lesions. All the cycasin-administered goats and 3 goats subacutely poisoned by cycad revealed vaculolar lesions in the central nervous system, which resembled spongy degeneration in the hepatocerebral syndrome in ruminants. By electron microscopy of the chronically intoxicated liver, both cycad and cycasin caused increase in number of mitochondria; cycad-poisoning induced marked enlargement of mitochondria, while cycasin-poisoning presented vacuolar dilatation of microsonal cysternae and electron dense pigments on the mass of smooth ER. Apoptotic changes were more severe in cycasin intoxication.
Further studies will be required for elucidation of role of cycasin in cycad-poisoning.
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