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哺乳动物细胞损伤导致不饱和脂肪酸氢过氧化物的酶促生成。

Enzymatic production of hydroperoxides of unsaturated fatty acids by injury of mammalian cells.

作者信息

Herold M, Spiteller G

机构信息

Institut fuer Organische Chemie I, Universitaet Bayreuth, Germany.

出版信息

Chem Phys Lipids. 1996 Mar 29;79(2):113-21. doi: 10.1016/0009-3084(95)02518-9.

Abstract

Hydroperoxides of unsaturated fatty acids (LOOHs) are generated by homogenisation of liver tissue, but not if the liver is boiled before homogenisation. This observation indicates that the LOOHs are produced in an enzymatic reaction. This assumption is corroborated by an analysis of the reduction products of LOOHs by gas chromatography/mass spectrometry (GC/MS). A main part of LOOHs is derived from linoleic acid and not from arachidonic acid. Massive cell damage occurs by myocardial infarction or other severe injuries; these events were found to be connected with generation of LOOHs. We suspect--considering the above outlined experiment--that the LOOH production is also mainly caused in these cases by activation of enzymes and not--as postulated--by an autocatalytic process. Increased amounts of LOOHs are found in many chronic diseases, e.g. in rheuma, atherosclerosis or psoriasis, obviously caused by a gradual damage of cells. Thus, the common root of an increased LOOH level might be cell injury.

摘要

不饱和脂肪酸的氢过氧化物(LOOHs)是通过肝脏组织匀浆产生的,但如果在匀浆前将肝脏煮沸则不会产生。这一观察结果表明,LOOHs是在酶促反应中产生的。通过气相色谱/质谱联用(GC/MS)对LOOHs的还原产物进行分析,证实了这一假设。LOOHs的主要部分来源于亚油酸而非花生四烯酸。心肌梗死或其他严重损伤会导致大量细胞损伤;这些事件被发现与LOOHs的产生有关。考虑到上述实验,我们怀疑在这些情况下,LOOH的产生也主要是由酶的激活引起的,而不是像假设的那样由自催化过程引起的。在许多慢性疾病中,如风湿、动脉粥样硬化或牛皮癣,发现LOOHs的含量增加,这显然是由细胞的逐渐损伤引起的。因此,LOOH水平升高的共同根源可能是细胞损伤。

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