缺血猪心脏组织中的脂质氧化产物。

Lipid oxidation products in ischemic porcine heart tissue.

作者信息

Dudda A, Spiteller G, Kobelt F

机构信息

Institut für Organische Chemie I, Universität Bayreuth, Germany.

出版信息

Chem Phys Lipids. 1996 Jul 30;82(1):39-51. doi: 10.1016/0009-3084(96)02557-1.

DOI:10.1016/0009-3084(96)02557-1

PMID:8810050

Abstract

Infarcted porcine heart tissue and surrounding tissue were investigated for the content of plasmalogens and oxidatively derived corresponding alpha-hydroxyaldehydes as well as for products of lipid peroxidation, e.g. malondialdehyde, glyoxal, 2-hydroxyheptanal and oxygenated fatty acids. Oxidation products of unsaturated fatty acids and plasmalogens were accumulated in infarcted tissue compared to the surrounding one. Their amounts increased with time of ischemia. In addition leukotoxins (9, 10-epoxy-12-octadecenoic acid and 12,13-epoxy-9-octadecenoic acid) as well as other epoxides of unsaturated fatty acids were identified. These compounds are absent in healthy heart tissue. Some of the monohydroxy fatty acids, found in comparable high yield, can not be derived from LPO processes. They are obviously generated from epoxides. Their distribution pattern indicates that they originate by an enzymic rather than by an autocatalytic process. We assume that the enzymes are activated by cell injury due to infarction. Linoleic acid seems to be an as equally well-suited substrate for enzymic attack as arachidonic acid.

摘要

对梗死猪心脏组织及其周围组织进行了研究，分析其中缩醛磷脂和氧化衍生的相应α-羟基醛的含量，以及脂质过氧化产物，如丙二醛、乙二醛、2-羟基庚醛和氧化脂肪酸。与周围组织相比，不饱和脂肪酸和缩醛磷脂的氧化产物在梗死组织中积累。其含量随缺血时间增加。此外，还鉴定出白细胞毒素（9,10-环氧-12-十八碳烯酸和12,13-环氧-9-十八碳烯酸）以及不饱和脂肪酸的其他环氧化物。这些化合物在健康心脏组织中不存在。一些以相当高产量发现的单羟基脂肪酸并非来自脂质过氧化过程。它们显然由环氧化物生成。其分布模式表明它们是通过酶促过程而非自催化过程产生的。我们推测这些酶因梗死导致的细胞损伤而被激活。亚油酸似乎与花生四烯酸一样是适合酶促攻击的底物。