ANTIOXIDANT ACTION OF UBIQUINOL HOMOLOGS WITH DIFFERENT ISOPRENOID CHAIN-LENGTH IN BIOMEMBRANES
ANTIOXIDANT ACTION OF UBIQUINOL HOMOLOGS WITH DIFFERENT ISOPRENOID CHAIN-LENGTH IN BIOMEMBRANES
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DOI：
10.1016/0891-5849(90)90114-x
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发表时间：
1990-01-01
影响因子：
7.4
通讯作者：
PACKER, L
中科院分区：
文献类型：
--
作者：
KAGAN, VE;SERBINOVA, EA;PACKER, L
泛醌（CoQn）是许多膜的固有脂质组分。除了它们在电子转移反应中的作用外，它们还可以作为自由基清除剂，但它们的抗氧化功能相对较少。在大鼠肝微粒体、脑突触体和线粒体中研究了不同类异戊二烯链长（从Q 0到Q10）的泛醇在预防（Fe 2 + +抗坏血酸盐）依赖性或（Fe 2 + + NADPH）依赖性脂质过氧化中的效率。 辅酶Qn的还原形式泛醌醇具有比氧化泛醌形式大得多的抗氧化活性。在均相溶液中，泛醇同系物的自由基清除活性不依赖于其类异戊二烯链的长度。然而，在膜中，具有短类异戊二烯链的泛醇（Q1-Q4）比长链同系物（Q5-Q10）更有效地抑制脂质过氧化。结果发现：i）短链泛醇的抑制作用，即抗氧化效率按Q1 > Q2 > Q3 > Q4的顺序降低; ii）长链泛醇的抗氧化效率仅轻微地依赖于它们的浓度，按Q5 > Q6 > Q7 > Q8 > Q9 > Q10的顺序降低; iii）Q 0的抗氧化效率明显低于其他同系物的抗氧化效率。泛醇与氧自由基的相互作用，其次是鲁米诺激活的化学发光的影响。0.1 mM的泛醌Q1-Q4完全抑制微粒体的鲁米诺激活的NADPH依赖性荧光反应，而同系物Q6-Q10不起作用。与泛醇Q10（泛醌Q10）相反，泛醌Q1协同增强微粒体中内源性维生素E的NADPH依赖性再生，从而提供针对脂质过氧化的更高的抗氧化保护。泛醇在膜中的抗氧化效力的差异被认为是由于泛醇在膜中的分配、膜内流动性和非均匀分布的差异导致与氧和脂质自由基的相互作用的不同效率以及泛醇在内源性维生素E的再生中的不同效率。
Ubiquinones (CoQn) are intrinsic lipid components of many membranes. Besides their role in electron-transfer reactions they may act as free radical scavengers, yet their antioxidant function has received relatively little study. The efficiency of ubiquinols of varying isoprenoid chain length (from Q0 to Q10) in preventing (Fe2+ + ascorbate)-dependent or (Fe2+ + NADPH)-dependent lipid peroxidation was investigated in rat liver microsomes and brain synaptosomes and mitochondria. Ubiquinols, the reduced forms of CoQn, possess much greater antioxidant activity than the oxidized ubiquinone forms. In homogenous solution the radical scavenging activity of ubiquinol homologues does not depend on the length of their isoprenoid chain. However in membranes ubiquinols with short isoprenoid chains (Q1-Q4) are much more potent inhibitors of lipid peroxidation than the longer chain homologues (Q5-Q10). It is found that: i) the inhibitory action, that is, antioxidant efficency of short-chain ubiquinols decreases in order Q1 > Q2 > Q3 > Q4; ii) the antioxidant efficiency of long-chain ubiquinols is only slightly dependent on their concentrations in the order Q5 > Q6 > Q7 > Q8 > Q9 > Q10 and iii) the antioxidant efficiency of Q0 is markedly less than that of other homologues. Interaction of ubiquinols with oxygen radicals was followed by their effects on luminol-activated chemiluminescence. Ubiquinols Q1-Q4 at 0.1 mM completely inhibit the luminol-activated NADPH-dependent chemiluminescent response of microsomes, while homologues Q6-Q10 exert no effect. In contrast to ubiquinol Q10 (ubiquinone Q10) ubiquinone Q1 synergistically enhances NADPH-dependent regeneration of endogenous vitamin E in microsomes thus providing for higher antioxidant protection against lipid peroxidation. The differences in the antioxidant potency of ubiquinols in membranes are suggested to result from differences in partitioning into membranes, intramembrane mobility and non-uniform distribution of ubiquinols resulting in differing efficiency of interaction with oxygen and lipid radicals as well as different efficiency of ubiquinols in regeneration of endogenous vitamin E.