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酗酒者体内自由基活性增加。

Increased free-radical activity in alcoholics.

作者信息

Fink R, Clemens M R, Marjot D H, Patsalos P, Cawood P, Norden A G, Iversen S A, Dormandy T L

出版信息

Lancet. 1985 Aug 10;2(8450):291-4. doi: 10.1016/s0140-6736(85)90347-2.

Abstract

The identification of the main dieneconjugated "free-radical marker" in human serum led to a study of free-radical activity in chronic alcoholics. 66 patients were investigated immediately after alcohol withdrawal and over 1-4 weeks' follow-up. The control groups were 76 normal subjects, 78 patients with liver disease, 30 patients on long-term antiepileptic drug treatment, 9 pregnant women, and 99 unselected hospital patients. 82% of chronic alcoholics had a significantly higher than normal level of phospholipid-esterified 9,11 linoleicacid isomer in blood collected within 24 h of their last alcoholic drink. The levels fell to normal over the next 2-4 days but continued to decline within the normal range for 2-3 weeks. There was no rise in the level of the isomer in normal controls after an acute alcohol load. The results suggest that chronic alcoholism may induce a specific detoxifying mechanism which is activated by alcohol and which entails or depends on greatly increased free-radical activity.

摘要

人血清中主要二烯共轭“自由基标志物”的鉴定引发了对慢性酗酒者自由基活性的研究。对66例患者在戒酒即刻及1至4周的随访期间进行了调查。对照组包括76名正常受试者、78名肝病患者、30名长期接受抗癫痫药物治疗的患者、9名孕妇以及99名未经过挑选的住院患者。82%的慢性酗酒者在最后一次饮酒后24小时内采集的血液中,磷脂酯化9,11 - 亚油酸异构体水平显著高于正常水平。在接下来的2至4天内,该水平降至正常,但在正常范围内又持续下降2至3周。急性酒精负荷后,正常对照组中该异构体水平未升高。结果表明,慢性酒精中毒可能诱导一种特定的解毒机制,该机制由酒精激活,且需要或依赖于自由基活性的大幅增加。

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