Gueux E, Azais-Braesco V, Bussière L, Grolier P, Mazur A, Rayssiguier Y
Centre de Recherche en Nutrition Humaine, Laboratoire des Maladies Métaboliques, INRA, St-Genès-Champanelle, France.
Br J Nutr. 1995 Dec;74(6):849-56.
Given the current interest in the cardiovascular complications of Mg deficiency, the aim of the present experiment was to investigate the effect of Mg deficiency on the time-course of lipoprotein oxidation and to assess whether short-term Mg deficiency results in vitamin E depletion that predisposes lipoproteins and tissues to subsequent oxidation. Weanling rats were pair-fed for 8 d with control and Mg-deficient diets respectively. Plasma triacylglycerol and alpha-tocopherol levels were significantly greater in Mg-deficient rats compared with control animals. The increase in plasma apolipoprotein B concentration indicated that a corresponding increase in plasma triacylglycerol-rich lipoproteins (TGRLP) occurred in Mg-deficient animals. Hyperlipaemia was associated with modifications in the composition of TGRLP. The proportion of triacylglycerols was elevated whereas that of cholesterol and protein was reduced, and Mg deficiency resulted in a slight significant reduction in alpha-tocopherol content. When the TGRLP fractions were subjected to in vitro Cu-induced oxidation the lipoprotein fractions from Mg-deficient rats were more susceptible to oxidative damage than lipoprotein fractions from control rats. Mg deficiency did not modify the alpha-tocopherol content of liver, heart and skeletal muscle. However, after exposure of tissue homogenates to Fe-induced lipid peroxidation, thiobarbituric acid-reactive substances were significantly higher in tissues from Mg-deficient rats compared with those from control rats. These results complement previous findings, showing that Mg deficiency increases the susceptibility of TGRLP and tissues to peroxidation and suggest that oxidative damage is not the result of a decrease in vitamin E antioxidant status.
鉴于目前对镁缺乏心血管并发症的关注，本实验旨在研究镁缺乏对脂蛋白氧化时间进程的影响，并评估短期镁缺乏是否会导致维生素E耗竭，从而使脂蛋白和组织易于随后的氧化。将断乳大鼠分别用对照饮食和缺镁饮食配对喂养8天。与对照动物相比，缺镁大鼠的血浆三酰甘油和α-生育酚水平显著更高。血浆载脂蛋白B浓度的增加表明缺镁动物血浆中富含三酰甘油的脂蛋白（TGRLP）相应增加。高脂血症与TGRLP组成的改变有关。三酰甘油的比例升高，而胆固醇和蛋白质的比例降低，并且镁缺乏导致α-生育酚含量略有显著降低。当TGRLP组分进行体外铜诱导氧化时，缺镁大鼠的脂蛋白组分比对照大鼠的脂蛋白组分更容易受到氧化损伤。镁缺乏并未改变肝脏、心脏和骨骼肌中的α-生育酚含量。然而，在将组织匀浆暴露于铁诱导的脂质过氧化后，与对照大鼠相比，缺镁大鼠组织中的硫代巴比妥酸反应性物质显著更高。这些结果补充了先前的发现，表明镁缺乏增加了TGRLP和组织对过氧化的敏感性，并表明氧化损伤不是维生素E抗氧化状态降低的结果。
