| Project/Area Number |
60560086
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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 |
応用生物化学・栄養化学
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| Research Institution | Nagoya University |
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Principal Investigator |
NAKANO Kiwao Nagoya University School of Agriculture, Assoc. Prof., 農学部, 助教授 (10023433)
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| Project Period (FY) |
1985 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1986: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1985: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Stress / Histamine / ヒスチジン脱炭素酵素 |
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| Research Abstract |
This study was carried out to investigate the mechanism of stress-induced tumorigenesis and to develop the nutritional methods for regulating the process. The results obtained are as follows:
i) Role of endogenous histamine in tumorigenesis: Histamine is known as one of the key substances in development of tumors. It is generally accepted that the amine is synthesized and released from mast cells and basophils. It is also known that the amine is formed through histidine decarboxylase in non-mast cells in response to mitogens or tumor promotor, TPA. However, no information is available on cells which are associated with induction of the enzyme. We have shown here, for the first time, that histidine decarboxylase is induced in macrophages with the aid of soluble factor(s)released from T lymphocytes (reports 1 - 7).
ii) Detoxification of histamine by ascorbic acid: Evidence is accumulated to indicate anti-tumor actions of ascorbic acid. The next study was to examine the mutual effects of histamine and ascorbic acid on immune reactions. The results obtained showed that during blastogenesis of mouse lymphocytes histamine was formed through histidine decarboxylase in the culture and that the lymphocyte transformation was suppressed by the amine. Addition of ascorbic acid to the culture caused decomposition of the endogenous histamine which led to derepression of the histamine-induced supression of the lymphocyte blastogenesis (reports 8,9).
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