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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >OLDER PLASMA LIPOPROTEINS ARE MORE SUSCEPTIBLE TO OXIDATION - A LINKING MECHANISM FOR THE LIPID AND OXIDATION THEORIES OF ATHEROSCLEROTIC CARDIOVASCULAR DISEASE
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OLDER PLASMA LIPOPROTEINS ARE MORE SUSCEPTIBLE TO OXIDATION - A LINKING MECHANISM FOR THE LIPID AND OXIDATION THEORIES OF ATHEROSCLEROTIC CARDIOVASCULAR DISEASE

机译：血浆中的旧脂蛋白更易被氧化-动脉粥样硬化性心血管疾病的脂质和氧化理论的联系机制

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Increases in plasma cholesterol are associated with progressive increases in the risk of atherosclerotic cardiovascular disease, In humans plasma cholesterol is contained primarily in apolipoprotein B-based low density lipoprotein (LDL). Cells stop making the high-affinity receptor responsible for LDL removal as they become cholesterol replete; this slows removal of LDL from plasma and elevates plasma LDL. As a result of this delayed uptake, hypercholesterolemic individuals not only have more LDL but have significantly older LDL. Oxidative modification of LDL enhances their atherogenicity. This study sought to determine whether increased time spent in circulation, or aging, by lipoprotein particles altered their susceptibility to oxidative modification, Controlled synchronous production of distinctive apolipoprotein B lipoproteins (yolk-specific very low density lipoproteins; VLDLy) with a single estrogen injection into young turkeys was used to model LDL aging in vivo. VLDLy remained in circulation for at least 10 days, Susceptibility to oxidation in vitro was highly dependent on lipoprotein age in vivo. Oxidation, measured as hexanal release from n-6 fatty acids in VLDLy: increased from 13.3 +/- 5.5 nmol of 2-day-old VLDLy per mi, to 108 +/- 17 nmol of 7-day-old VLDLy per mi, Oxidative instability was not due to tocopherol depletion or conversion to a more unsaturated fatty acid composition, These findings establish mathematically describable linkages between the variables of LDL concentration and LDL oxidation. The proposed mathematical models suggest a unified investigative approach to determine the mechanisms for acceleration of atherosclerotic cardiovascular disease risk as plasma cholesterol rises. [References: 47]
机译：血浆胆固醇的增加与动脉粥样硬化性心血管疾病风险的逐步增加有关。在人类中，血浆胆固醇主要包含在基于载脂蛋白B的低密度脂蛋白（LDL）中。当细胞变得胆固醇充足时，细胞就会停止制造负责LDL去除的高亲和力受体。这减慢了血浆中LDL的去除并提高了血浆LDL。由于这种延迟摄取，高胆固醇血症的个体不仅具有更多的LDL，而且具有明显更老的LDL。 LDL的氧化修饰可增强其动脉粥样硬化性。这项研究试图确定脂蛋白颗粒是否增加了循环或老化所花费的时间，从而改变了其对氧化修饰的敏感性，通过单一雌激素注射控制了同步生产独特的载脂蛋白B脂蛋白（卵黄特异性极低密度脂蛋白； VLDLy）。幼小的火鸡被用来模拟体内低密度脂蛋白的衰老。 VLDLy保持循环至少10天，体外氧化的敏感性高度依赖于体内脂蛋白的年龄。以VLDLy中n-6个脂肪酸的己醛释放量衡量的氧化：从每英里2天大的VLDLy的13.3 +/- 5.5 nmol增加到每英里7天大的VLDLy的108 +/- 17 nmol，氧化不稳定性不是由于生育酚消耗或转化为更不饱和的脂肪酸组成所致。这些发现在LDL浓度和LDL氧化变量之间建立了数学上可描述的联系。提出的数学模型提出了一种统一的研究方法，以确定随着血浆胆固醇升高而加速动脉粥样硬化性心血管疾病风险的机制。 [参考：47]

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