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大鼠小肠缺血后脂质过氧化产物4-羟基壬烯醛的蓄积

Postischemic accumulation of the lipid peroxidation product 4-hydroxynonenal in rat small intestine.

作者信息

Grune T, Siems W G, Kowalewski J, Esterbauer H

机构信息

Clinic of Physical Therapy and Rehabilitation, Medical Faculty (Charité), Humboldt University Berlin, Germany.

出版信息

Life Sci. 1994;55(9):693-9. doi: 10.1016/0024-3205(94)00676-8.

DOI:10.1016/0024-3205(94)00676-8
PMID:7848414
Abstract

4-Hydroxynonenal (HNE) as an indicator of lipid peroxidation was determined in rat jejunal mucosa. HNE was extracted as the dinitrophenylhydrazone derivative from the tissue, partially separated from other carbonyl compounds by thin-layer chromatography and measured by HPLC. During reperfusion of the small intestine following an ischemic period of 60 minutes a marked increase of the tissue concentration of HNE was observed. The mucosal HNE level passed a maximum value of 3.0 +/- 0.5 microM 10 min after the onset of reperfusion in comparison with 0.7 +/- 0.2 microM as initial value. The increased tissue level of the highly cytotoxic 4-hydroxyalkenal is suggested to be involved in the reperfusion induced morphological and biochemical changes of the small intestine.

摘要

在大鼠空肠黏膜中测定了作为脂质过氧化指标的4-羟基壬烯醛(HNE)。HNE作为二硝基苯腙衍生物从组织中提取出来,通过薄层色谱法与其他羰基化合物部分分离,并通过高效液相色谱法进行测定。在60分钟缺血期后的小肠再灌注过程中,观察到HNE的组织浓度显著增加。与初始值0.7±0.2微摩尔相比,再灌注开始10分钟后,黏膜HNE水平达到3.0±0.5微摩尔的最大值。高细胞毒性的4-羟基烯醛组织水平升高被认为与再灌注诱导的小肠形态和生化变化有关。

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Redox signaling: An evolution from free radicals to aging.氧化还原信号传导:从自由基到衰老的演变。
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4-Hydroxynonenal increases gamma-glutamyl transpeptidase gene expression through mitogen-activated protein kinase pathways.4-羟基壬烯醛通过丝裂原活化蛋白激酶途径增加γ-谷氨酰转肽酶基因表达。
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Evaluation of purine nucleotide loss, lipid peroxidation and ultrastructural alterations in post-hypoxic hepatocytes.
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J Physiol. 1997 Jan 15;498 ( Pt 2)(Pt 2):511-22. doi: 10.1113/jphysiol.1997.sp021877.