Reaction of phosphatidylcholine hydroperoxide in human plasma: the role of peroxidase and lecithin:cholesterol acyltransferase.
Reaction of phosphatidylcholine hydroperoxide in human plasma: the role of peroxidase and lecithin:cholesterol acyltransferase.
复制标题
人血浆中磷脂酰胆碱过氧化氢的反应：过氧化物酶和卵磷脂的作用：胆固醇酰基转移酶。
DOI：
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发表时间：
1996
影响因子：
3.9
通讯作者：
E. Niki
中科院分区：
文献类型：
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作者：
Y. Nagata;Y. Yamamoto;E. Niki
为了阐明过氧化磷脂酰胆碱在人血浆中不稳定的原因，将1-棕榈酰-2-亚油基过氧化磷脂酰胆碱（PLPC-OOH）在人血浆中37℃有氧培养，并测定其分解产物。主要产物是相应的醇（PLPC-OH），这种减少可能是通过酶促过程发生的，因为添加PLPC-OOH后，抗坏血酸消耗没有加速，其他血浆抗氧化剂也没有显著减少。过氧化亚油酸胆固醇及其醇（Ch18:2-OH）也是次要产物。同样，1-硬脂酰-2-花生四烯酰基磷脂酰胆碱过氧化氢的主要产物是醇（SAPC-OH），次要产物是花生四烯酸胆固醇及其氢氧化物（Ch20:4=OH）。这些氧化的胆固醇酯可能是由卵磷脂的作用产生的：高密度脂蛋白（HDL）中存在胆固醇酰基转移酶（LCAT），因为(a)人血浆中PLPC-OH和SAPC-OH分别产生Ch18:2-OH和Ch20:4-OH， (b)分离的人HDL将PLPC-OH转化为Ch18:2 OH和SAPC-OH转化为Ch20:4-OH，而分离的人低密度脂蛋白对这种转化无活性。(c) LCAT抑制剂5,5'-二硫代obis（2-硝基苯甲酸）抑制血浆和HDL中氧化胆固醇酯的形成。还讨论了LCAT在将过氧化磷脂酰胆碱转化为过氧化胆固醇酯的过程中可能发挥的有益作用。
In order to elucidate the reason why phosphatidylcholine hydroperoxide is unstable in human plasma, 1-palmitoyl-2-linoleoylphosphatidylcholine hydroperoxide (PLPC-OOH) was incubated aerobically in human plasma at 37 degrees C, and its decomposition products were measured. The major product was the corresponding alcohol (PLPC-OH) and this reduction probably occurred by an enzymatic process since no acceleration in ascorbate depletion and no significant decrease in other plasma antioxidants were observed upon addition of PLPC-OOH. Cholesteryl linoleate hydroperoxide and its alcohol (Ch18:2-OH) were also detected as minor products. Similarly, 1-stearoyl-2-arachidonoylphosphatidylcholine hydroperoxide gave its alcohol (SAPC-OH) as a major product and cholesteryl arachidonate hydroperoxide and its hydroxide (Ch20:4=OH) as minor products. These oxidized cholesteryl esters are likely to be produced by the action of lecithin:cholesterol acyltransferase (LCAT) present in high-density lipoprotein (HDL) since (a) incubation of PLPC-OH and SAPC-OH in human plasma gave Ch18:2-OH and Ch20:4-OH, respectively, (b) isolated human HDL converted PLPC-OH to Ch18:2 OH and SAPC-OH to Ch20:4-OH while isolated human low-density lipoprotein was inactive for this conversion, and (c) formation of oxidized cholesteryl esters in plasma and HDL was inhibited by the LCAT inhibitor 5,5'-dithiobis(2-nitrobenzoic acid). A possible beneficial role of LCAT for converting phosphatdylcholine hydroperoxide to cholesteryl ester hydroperoxide is also discussed.