Reaven P D, Ferguson E, Navab M, Powell F L
Division of Endocrinology and Metabolism, University of California, San Diego 92093-0682.
Arterioscler Thromb. 1994 Jul;14(7):1162-9. doi: 10.1161/01.atv.14.7.1162.
Epidemiological studies suggest that beta-carotene supplementation may decrease atherosclerotic events. Because beta-carotene is transported in low-density lipoprotein (LDL), one mechanism by which this protective effect may occur is through direct inhibition of LDL oxidation. Addition of beta-carotene to LDL in vitro inhibits the susceptibility of LDL to oxidation. In contrast, we have shown that feeding large doses of beta-carotene results in beta-carotene-enriched plasma LDL (16- to 35-fold), but such LDL does not show increased resistance to oxidation. Potential criticisms of our initial study relate to the unique antioxidant properties of beta-carotene. Beta-Carotene provides better quenching of some free radicals, such as singlet oxygen, than others. Additionally, since beta-carotene can easily autooxidize, forming metabolites that can also generate free radicals, it has been argued that at sufficient concentrations in vivo the antioxidant effect of beta-carotene may be diminished. It has thus been suggested that in our initial study we may have failed to properly assess the unique antioxidant effects of beta-carotene by our selection of oxidizing conditions and/or failed to achieve antioxidant activity because of excessive enrichment of LDL with beta-carotene. We now report the effects of feeding lower doses of beta-carotene on the susceptibility of LDL to oxidation and test whether any antioxidant activity of beta-carotene can be detected when different modes of initiating oxidation are used. Because the antioxidant activity of beta-carotene is reputedly most pronounced in low-oxygen environments, we also investigated its effect on LDL oxidation under conditions of reduced oxygen tension.(ABSTRACT TRUNCATED AT 250 WORDS)
流行病学研究表明，补充β-胡萝卜素可能会减少动脉粥样硬化事件。由于β-胡萝卜素是通过低密度脂蛋白（LDL）运输的，这种保护作用可能发生的一种机制是直接抑制LDL氧化。在体外向LDL中添加β-胡萝卜素可抑制LDL的氧化敏感性。相比之下，我们已经表明，喂食大剂量的β-胡萝卜素会导致血浆中富含β-胡萝卜素的LDL（增加16至35倍），但这种LDL对氧化的抵抗力并未增加。对我们最初研究的潜在批评与β-胡萝卜素独特的抗氧化特性有关。β-胡萝卜素对某些自由基（如单线态氧）的淬灭效果比其他自由基更好。此外，由于β-胡萝卜素很容易自动氧化，形成的代谢产物也能产生自由基，有人认为在体内足够浓度时，β-胡萝卜素的抗氧化作用可能会减弱。因此有人提出，在我们最初的研究中，我们可能由于选择的氧化条件而未能正确评估β-胡萝卜素独特的抗氧化作用，和/或由于LDL中β-胡萝卜素过度富集而未能实现抗氧化活性。我们现在报告喂食较低剂量β-胡萝卜素对LDL氧化敏感性的影响，并测试在使用不同氧化引发方式时是否能检测到β-胡萝卜素的任何抗氧化活性。由于据说β-胡萝卜素的抗氧化活性在低氧环境中最为明显，我们还研究了其在低氧张力条件下对LDL氧化的影响。（摘要截断于250字）
