Mechanism of Ethanol Degradation and Production in Intestinal Tract
Mechanism of Ethanol Degradation and Production in Intestinal Tract
批准号:
01570345
负责人:
TANAKA Noriyuki
金额:
$1.22万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for General Scientific Research (C)
财政年份:
1989
资助国家:
日本
项目状态:
已结题
起止时间:
1989 至 1990
中文摘要
本研究通过体外和体内对家兔肠道内容物进行细菌学检查,阐明乙醇代谢在家兔肠道中的作用机制。在体内研究表明,乙醇在盲肠、结肠和直肠的内容物中被降解和产生。乙醇脱氢酶参与了盲肠内容物中乙醇的降解。过氧化氢酶对其降解作用不大。这些酶是由肠道细菌产生的,在体内受到氯霉素和粘菌素的影响。盲肠内容物中乙醇的降解占体内乙醇降解总量的3.5%。在体外研究中,肠道细菌被证明可以降解并产生乙醇。乙醇脱氢酶和过氧化氢酶介导大肠杆菌对乙醇的体外降解。具有降解乙醇能力的肠道细菌被氯霉素、链霉素和粘菌素抑制繁殖。结果表明,这些抗生素对乙醇降解的降低可能是抑制肠道细菌繁殖的结果。
英文摘要
In this study, the intestinal tract contents in rabbit were examined bacteriologically in vitro and in vivo to clarify the mechanism of ethanol metabolism in it.1. In vivo study, it was demonstrated that ethanol was degraded and produced in the contents of cecum, colon and rectum.2. Alcohol dehydrogenase participated in the ethanol degradation in cecum content. Catalase had little effect on the degradation.3. These enzymes were created by enteric bacteria, and affected by chloramphenicol and colistin in vivo.4. The ethanol degradation in cecum content accounted for 3.5% of all ethanol degradation in vivo.5. In vitro study, enteric bacteria was demonstrated to degrade and produce the ethanol.6. The ethanol degradation of enteric bacteria (E. Coli) in vitro was mediated by alcohol dehydrogenase and catalase.The enteric bacteria that had a ability to degrade the ethanol was inhibited to multiply by chloramphenicol, streptomycin and colistin. It was suggested that the decrease of ethanol degradation by these antibiotics was the result of the inhibition to multiply the enteric bacteria.
期刊论文(3)
专著(0)
科研奖励(0)
会议论文
田中 宣幸: "家兎腸管内におけるアルコ-ル分解および産生のメカニズム" 日本法医学雑誌.
Nobuyuki Tanaka:“家兔肠道中酒精分解和产生的机制”日本法医学杂志。
DOI:
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发表时间:
期刊:
影响因子:
--
作者:
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通讯作者:
Noriyuki Tanaka: "Studies on the ethanol metabolism in intestine of rabbit." Jpn J Legal Med.
Noriyuki Tanaka:“兔子肠道中乙醇代谢的研究。”
DOI:
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发表时间:
期刊:
影响因子:
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作者:
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通讯作者:
A study of neutrophils on diagnosis of the severity in organ dysfunction and the cause of death following hemorrhagic shock
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批准号:20590692
-
项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$1.25万
-
财政年份:2008
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负责人:TANAKA Noriyuki
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依托单位:
Mechanisms of cardiac dysfunction induced by hemorrhagic shock
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批准号:17590589
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财政年份:2005
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负责人:TANAKA Noriyuki
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依托单位:
The role of cytokine and nitric oxide on multiple organ failures in hemorrhagic shock
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批准号:12470110
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项目类别:Grant-in-Aid for Scientific Research (B)
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资助金额:$2.75万
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财政年份:2000
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依托单位:
The mechanism of diffuse axonal injury development
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批准号:09670460
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财政年份:1997
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依托单位:
Behavior of N2O in the atmosphere and making the global budget using nitrogen and oxygen isotope systematics
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批准号:07454136
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资助金额:$4.93万
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财政年份:1995
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依托单位:
The role of chemical mediator on the occurrence of brain edema after traumatic head injury
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资助金额:$2.11万
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财政年份:1995
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负责人:TANAKA Noriyuki
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依托单位:
Studies on the Endotoxin Shock
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批准号:03670309
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项目类别:Grant-in-Aid for General Scientific Research (C)
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资助金额:$1.22万
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财政年份:1991
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负责人:TANAKA Noriyuki
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依托单位:
海外基金