Gatica Laura V, Vega Verónica A, Zirulnik Fanny, Oliveros Liliana B, Gimenez María S
Department of Biochemistry and Biological Sciences, Faculty of Chemistry, Biochemistry and Pharmacy, National University of San Luis, San Luis, Argentina.
J Vasc Res. 2006;43(6):602-10. doi: 10.1159/000096247. Epub 2006 Oct 13.
Antioxidants are known to reduce cardiovascular disease by reducing the concentration of free radicals in the vessel wall and by preventing the oxidative modification of low-density lipoproteins. The prooxidative effect of a vitamin-A-deficient diet on the aorta has previously been demonstrated by us. In this study, the lipid metabolism in the aorta of rats fed on a vitamin-A-deficient diet was evaluated. Vitamin A deficiency induced a hypolipidemic effect (lower serum triglyceride and cholesterol levels) and a decreased serum paraoxonase 1/arylesterase activity. The concentrations of triglycerides, total cholesterol, free and esterified cholesterol, and phospholipids were increased in the aorta of vitamin-A-deficient rats. The phospholipid compositions showed an increase in phosphatidylcholine (PC), phosphatidylinositol plus phosphatidylserine and phosphatidylethanolamine, a decrease in sphingomyelin, and no change in phosphatidylglycerol. In the aorta, the increase in triglycerides was associated with an increased fatty acid synthesis and mRNA expression of diacylglycerol acyltransferase 1. The increased PC content was attributed to an increased synthesis, as measured by [methyl-(14)C]choline incorporation into PC and high CTP:phosphocholine cytidylyltransferase-alpha mRNA expression. The cholesterol synthesis, evaluated by [1-(14)C]acetate incorporated into cholesterol and mRNA expression of 3-hydroxy-3-methylglutaryl coenzyme A reductase, did not change. The lipoprotein lipase and lectin-like oxidized low-density lipoprotein receptor 1 mRNA expression levels increased in the aorta of vitamin-A-deficient animals. The incorporation of vitamin A into the diet of vitamin-A-deficient rats reverted all the changes observed. These results indicate that a vitamin-A-deficient diet,in addition to having a prooxidative effect, alters the aorta lipid metabolism.
众所周知，抗氧化剂可通过降低血管壁中自由基的浓度以及防止低密度脂蛋白的氧化修饰来降低心血管疾病风险。我们之前已经证明了维生素A缺乏饮食对主动脉的促氧化作用。在本研究中，对喂食维生素A缺乏饮食的大鼠主动脉中的脂质代谢进行了评估。维生素A缺乏会导致低脂血症（血清甘油三酯和胆固醇水平降低）以及血清对氧磷酶1/芳基酯酶活性降低。维生素A缺乏的大鼠主动脉中甘油三酯、总胆固醇、游离胆固醇和酯化胆固醇以及磷脂的浓度均升高。磷脂组成显示磷脂酰胆碱（PC）、磷脂酰肌醇加磷脂酰丝氨酸和磷脂酰乙醇胺增加，鞘磷脂减少，磷脂酰甘油无变化。在主动脉中，甘油三酯的增加与脂肪酸合成增加和二酰基甘油酰基转移酶1的mRNA表达增加有关。PC含量的增加归因于合成增加，这通过[甲基 - （14）C]胆碱掺入PC以及高CTP：磷酸胆碱胞苷转移酶 - α mRNA表达来衡量。通过[1 - （14）C]乙酸掺入胆固醇以及3 - 羟基 - 3 - 甲基戊二酰辅酶A还原酶的mRNA表达评估的胆固醇合成没有变化。维生素A缺乏动物的主动脉中脂蛋白脂肪酶和凝集素样氧化低密度脂蛋白受体1的mRNA表达水平增加。在维生素A缺乏的大鼠饮食中添加维生素A可逆转所有观察到的变化。这些结果表明，维生素A缺乏饮食除了具有促氧化作用外，还会改变主动脉脂质代谢。
