Stadelmann-Ingrand Sabrina, Pontcharraud Raymond, Fauconneau Bernard
EA 3808, Faculté de Médecine Pharmacie, 34 rue du Jardin des Plantes, BP 199, 86005 Poitiers, France.
Chem Phys Lipids. 2004 Aug;131(1):93-105. doi: 10.1016/j.chemphyslip.2004.04.008.
The vinyl ether bond of plasmalogens could be among the first target of free radicals attack. Consequently, because of their location in the membranes of cells, plasmalogens represent a first shield against oxidative damages by protecting other macromolecules and are often considered as antioxidant molecules. However, under oxidative conditions their disruption leads to the release of fatty aldehydes. In this paper, we showed using gas chromatography-mass spectrometry (GC-MS) analyses that fatty aldehydes released from plasmalogens after oxidation (UV irradiation and Fe2+/ascorbate) of cerebral cortex homogenates can generate covalent modifications of endogenous macromolecules such as phosphatidylethanolamine (PE), like the very reactive and toxic malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE). These newly formed Schiff base adducts could be responsible for deleterious effects on cells thus making the protective role of plasmalogens potentially questionable.
缩醛磷脂的乙烯醚键可能是自由基攻击的首批靶点之一。因此，由于它们存在于细胞膜中，缩醛磷脂通过保护其他大分子，成为抵御氧化损伤的第一道屏障，常被视为抗氧化分子。然而，在氧化条件下，它们的分解会导致脂肪醛的释放。在本文中，我们通过气相色谱 - 质谱联用（GC-MS）分析表明，大脑皮层匀浆在氧化（紫外线照射和Fe2+/抗坏血酸盐）后从缩醛磷脂释放的脂肪醛可对内源性大分子如磷脂酰乙醇胺（PE）产生共价修饰，就像极具反应性和毒性的丙二醛（MDA）和4-羟基壬烯醛（4-HNE）一样。这些新形成的席夫碱加合物可能对细胞产生有害影响，从而使缩醛磷脂的保护作用可能受到质疑。
