Gaziano J M, Hatta A, Flynn M, Johnson E J, Krinsky N I, Ridker P M, Hennekens C H, Frei B
Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA.
Atherosclerosis. 1995 Jan 20;112(2):187-95. doi: 10.1016/0021-9150(94)05414-e.
The inhibition of low density lipoprotein (LDL) oxidation has been postulated as one mechanism by which antioxidants may prevent the development of atherosclerosis. Available data on the ability of beta-carotene to inhibit LDL oxidation are conflicting. We examined the role of in vivo and in vitro supplementation with beta-carotene on metal ion-dependent (cupric ions, Cu2+) and metal ion-independent (2,2'-azobis[2-amidinopropane]dihydrochloride, AAPH) oxidation of LDL as measured by the formation of conjugated dienes (absorbance at 234 nm). Sixteen subjects were supplemented with 50-100 mg of beta-carotene on alternate days for 3 weeks following a week-long loading dose of 100 mg/day. Plasma beta-carotene levels rose 5.5-fold, while LDL beta-carotene levels rose 8.5-fold. Oxidation of LDL by Cu2+ or AAPH was not significantly delayed after in vivo supplementation with beta-carotene compared with baseline. For AAPH, the lag phase (in minutes) was 75 +/- 8 at baseline and 83 +/- 14 after supplementation (P = 0.07). For Cu2+, the lag phase was 172 +/- 41 at baseline and decreased to 130 +/- 24 after supplementation (P < 0.01). Similarly, no protective effect against Cu(2+)-induced oxidation was observed when beta-carotene was added to LDL in vitro. Supplementation of plasma with beta-carotene in vitro prior to LDL isolation also did not enhance LDL's resistance to Cu(2+)- or AAPH-induced oxidation, despite a 5-fold increase in LDL beta-carotene levels over vehicle control.(ABSTRACT TRUNCATED AT 250 WORDS)
低密度脂蛋白(LDL)氧化的抑制作用被认为是抗氧化剂预防动脉粥样硬化发展的一种机制。关于β-胡萝卜素抑制LDL氧化能力的现有数据相互矛盾。我们研究了体内和体外补充β-胡萝卜素对LDL金属离子依赖性(铜离子,Cu2+)和金属离子非依赖性(2,2'-偶氮二[2-脒基丙烷]二盐酸盐,AAPH)氧化的作用,通过共轭二烯的形成(234nm处的吸光度)来测量。16名受试者在每天服用100mg的一周负荷剂量后,每隔一天补充50-100mg的β-胡萝卜素,持续3周。血浆β-胡萝卜素水平升高了5.5倍,而LDLβ-胡萝卜素水平升高了8.5倍。与基线相比,体内补充β-胡萝卜素后,Cu2+或AAPH对LDL的氧化并未显著延迟。对于AAPH,基线时的延迟期(以分钟计)为75±8,补充后为83±14(P = 0.07)。对于Cu2+,基线时的延迟期为172±41,补充后降至130±24(P < 0.01)。同样,体外将β-胡萝卜素添加到LDL中时,未观察到对Cu(2+)诱导氧化的保护作用。在分离LDL之前体外向血浆中补充β-胡萝卜素,也未增强LDL对Cu(2+)或AAPH诱导氧化的抵抗力,尽管LDLβ-胡萝卜素水平比载体对照增加了5倍。(摘要截短至250字)