Uto-Kondo Harumi, Kiyose Chikako, Ohmori Reiko, Saito Hisako, Taguchi Chie, Kishimoto Yoshimi, Machida Naoko, Hasegawa Maiko, Yoshioka Eri, Saita Emi, Hirata Yumiko, Igarashi Osamu, Kondo Kazuo
Institute of Environmental Science for Human Life, Ochanomizu University, Tokyo 112-8610, Japan.
J Nutr Sci Vitaminol (Tokyo). 2007 Aug;53(4):301-5. doi: 10.3177/jnsv.53.301.
alpha-Tocopherol (alpha-Toc) is abundant in LDL and thought to prevent the oxidation of LDL together with various water-soluble antioxidants. Recently, it was reported that alpha-Toc and gamma-Toc metabolites, alpha-carboxyethyl-6-hydroxychromans (CEHC) and gamma-CEHC, are water-soluble antioxidants. In this study, we investigated the interaction between alpha-Toc and CEHC against 1,1-diphenyl-2-picryl-hydrazyl (DPPH) radicals and LDL oxidation. We administered 600 mg of alpha-Toc to healthy male volunteers to obtain LDL including high levels of alpha-Toc before antioxidant administration. The alpha-Toc content of their LDL was increased after consumption at 24 h (18.3 microg/mL) above the level before consumption (6.6 microg/mL). The lag time of LDL at 24 h after alpha-Toc consumption (alpha-Toc rich LDL) with alpha-CEHC (98.5+/-8.2 min) or gamma-CEHC (101.3+/-9.0 min) was longer than that of only alpha-Toc-rich LDL (78.1+/-9.0 min). Furthermore, we examined the interaction of LDL with CEHC and alpha-Toc in vitro (5-20 microg/mL). The lag times of 5 and 10 microg/mL alpha-Toc were 65.5+/-18.9 min and 69.5+/-15.5 min, and that of 20 microg/mL alpha-Toc (83.5+/-20.2 min) was longer than the control value (55.7+/-14.1 min). The lag time of 20 microg/mL alpha-Toc with alpha-CEHC (98.7+/-25.7 min) or gamma-CEHC (100.6+/-25.3 min) was longer than that of only alpha-Toc (83.5+/-20.2 min). These results suggest that CEHC has the potential to delay the oxidation of LDL, while enhancing the antioxidative activity of alpha-Toc both in vitro and ex vivo.
α-生育酚(α-Toc)在低密度脂蛋白(LDL)中含量丰富,被认为可与多种水溶性抗氧化剂共同预防LDL的氧化。最近有报道称,α-Toc和γ-Toc的代谢产物α-羧乙基-6-羟基色满(CEHC)和γ-CEHC是水溶性抗氧化剂。在本研究中,我们研究了α-Toc与CEHC针对1,1-二苯基-2-苦基肼(DPPH)自由基和LDL氧化的相互作用。我们给健康男性志愿者服用600毫克α-Toc,以获取抗氧化剂给药前α-Toc含量高的LDL。服用后24小时,他们LDL中的α-Toc含量增加(18.3微克/毫升),高于服用前水平(6.6微克/毫升)。服用α-Toc后24小时(富含α-Toc的LDL)与α-CEHC(98.5±8.2分钟)或γ-CEHC(101.3±9.0分钟)共同作用时,LDL的延迟时间比仅富含α-Toc的LDL(78.1±9.0分钟)更长。此外,我们在体外(5 - 20微克/毫升)研究了LDL与CEHC和α-Toc的相互作用。5微克/毫升和10微克/毫升α-Toc的延迟时间分别为65.5±18.9分钟和69.5±15.5分钟,20微克/毫升α-Toc的延迟时间(83.5±20.2分钟)长于对照值(55.7±14.1分钟)。20微克/毫升α-Toc与α-CEHC(98.7±25.7分钟)或γ-CEHC(100.6±25.3分钟)共同作用时的延迟时间比仅α-Toc(83.5±20.2分钟)更长。这些结果表明,CEHC有延缓LDL氧化的潜力,同时在体外和体内均能增强α-Toc的抗氧化活性。