Peroxidation of membrane phospholipids is an important determinant of membrane function. Previously we studied the kinetics of peroxidation of the polyunsaturated fatty acid (PUFA) residues in model membranes (liposomes) made by sonication of palmitoyllinoleoylphosphatidylcholine (PLPC). Since most biomembranes are negatively-charged, we have now studied the effect of negative surface charge on the kinetics of peroxidation of liposomes made of PLPC and 9% of one of the negatively-charged phospholipids phosphatidylserine (PS) or phosphatidic acid (PA). Peroxidation was initiated by either CuCl2 or AAPH and continuously monitored spectrophotometrically. The following results were obtained: (i) The negative charge had only a slight effect on AAPH-induced peroxidation, but accelerated markedly copper-induced peroxidation of the liposomes, probably by increasing the binding of copper to the membrane surface. (ii) Ascorbic acid (AA) inhibited AAPH-induced but promoted copper-induced peroxidation in all the studied liposomes, probably by enhancing the production of free radicals upon reduction of Cu(II) to Cu(I). (iii) alpha-tocopherol (Toc) inhibited AAPH-induced peroxidation in all the studied liposomes, whereas the effect of tocopherol on copper-induced peroxidation varied from being pro-oxidative in PA-containing liposomes, to being extremely anti-oxidative in PS-containing liposomes, even at very low tocopherol concentrations. The significance of the latter unusual protective effect, which we attribute to recycling of tocopherol by a PS-Cu complex, requires further investigation.

中文翻译：

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脂质体棕榈酰亚油酰基磷脂酰胆碱（PLPC）的过氧化作用，表面电荷对氧化性和抗氧化剂效能的影响。

膜磷脂的过氧化作用是膜功能的重要决定因素。以前，我们研究了通过超声处理棕榈酰亚油酰基磷脂酰胆碱（PLPC）制成的模型膜（脂质体）中多不饱和脂肪酸（PUFA）残基的过氧化动力学。由于大多数生物膜带有负电荷，因此我们现在研究了负表面电荷对PLPC和9％的负电荷磷脂酰丝氨酸（PS）或磷脂酸（PA）中的一种脂质体的过氧化动力学的影响。过氧化作用由CuCl2或AAPH引发，并通过分光光度法连续监控。获得了以下结果：（i）负电荷对AAPH诱导的过氧化反应仅产生轻微影响，但明显加速了铜诱导的脂质体的过氧化反应，可能是通过增加铜与膜表面的结合力来实现的。（ii）在所有研究的脂质体中，抗坏血酸（AA）抑制了AAPH诱导但促进了铜诱导的过氧化，可能是通过将Cu（II）还原为Cu（I）来增强自由基的产生。（iii）α-生育酚（Toc）在所有研究的脂质体中均抑制AAPH诱导的过氧化，而生育酚对铜诱导的过氧化的作用从含PA脂质体中的前氧化到PS中极度抗氧化的变化含脂质体，即使生育酚浓度很低也是如此。后一种异常保护作用的重要性（我们归因于PS-Cu络合物回收生育酚）需要进一步研究。（ii）在所有研究的脂质体中，抗坏血酸（AA）抑制了AAPH诱导但促进了铜诱导的过氧化，可能是通过将Cu（II）还原为Cu（I）来增强自由基的产生。（iii）α-生育酚（Toc）在所有研究的脂质体中均抑制AAPH诱导的过氧化，而生育酚对铜诱导的过氧化的作用从含PA脂质体中的前氧化到PS中极度抗氧化的变化含脂质体，即使生育酚浓度很低也是如此。后一种异常保护作用的重要性（我们归因于PS-Cu络合物回收生育酚）需要进一步研究。（ii）在所有研究的脂质体中，抗坏血酸（AA）抑制了AAPH诱导但促进了铜诱导的过氧化，可能是通过将Cu（II）还原为Cu（I）来增强自由基的产生。（iii）α-生育酚（Toc）在所有研究的脂质体中均抑制AAPH诱导的过氧化，而生育酚对铜诱导的过氧化的作用从含PA脂质体中的前氧化到PS中极度抗氧化的变化含脂质体，即使生育酚浓度很低也是如此。后一种异常保护作用的重要性（我们归因于PS-Cu络合物回收生育酚）需要进一步研究。（iii）α-生育酚（Toc）在所有研究的脂质体中均抑制AAPH诱导的过氧化，而生育酚对铜诱导的过氧化的作用从含PA脂质体中的前氧化到PS中的极度抗氧化含脂质体，即使生育酚浓度很低也是如此。后一种异常保护作用的重要性（我们归因于PS-Cu络合物回收生育酚）需要进一步研究。（iii）α-生育酚（Toc）在所有研究的脂质体中均抑制AAPH诱导的过氧化，而生育酚对铜诱导的过氧化的作用从含PA脂质体中的前氧化到PS中极度抗氧化的变化含脂质体，即使生育酚浓度很低也是如此。后一种异常保护作用的重要性（我们归因于PS-Cu络合物回收生育酚）需要进一步研究。