Effect of hydroxytyrosol found in extra virgin olive oil on oxidative DNA damage and oil low-density lipoprotein oxidation

被引:115
作者
Aruoma, OI
Deiana, M
Jenner, A
Halliwell, B
Kaur, H
Banni, S
Corongiu, FP
Dessí, MA
Aeschbach, R
机构
[1] Univ Sao Paulo, Fac Pharmaceut Sci, Dept Clin Anal Toxicol & Bromatol, BR-14040903 Ribeirao Preto, Brazil
[2] Univ London, Univ London Kings Coll, Pharmacol Grp, London SW3 6LX, England
[3] Univ Cagliari, Dipartimento Biol Sperimentale, Sez Patol Sperimentale, I-09040 Cagliari, Italy
[4] Natl Univ Singapore, Dept Biochem, Singapore 119260, Singapore
[5] Northwick Pk Inst Med Res, Dept Surg Res, Vasc Biol Unit, Harrow HA1 3UJ, Middx, England
[6] Nestle Res Ctr, CH-1000 Lausanne 26, Switzerland
关键词
extra virgin olive oil; hydroxytyrosol; low-density lipoprotein; rosemary; vitamin E; lipid peroxidation; plant antioxidants; DNA damage;
D O I
10.1021/jf980649b
中图分类号
S [农业科学];
学科分类号
09 ;
摘要
Hydroxytyrosol found in extra virgin olive oil strongly inhibited low-density lipoprotein oxidation stimulated by 2,2'-azobis(2-amidinopropane) hydrochloride (AAPH), suggesting the ability to scavenge the AAPH-derived peroxyl radicals. Hydroxytyrosol inhibited iron-dependent phospholipid Liposome peroxidation at low concentrations (IC50 = 50 +/- 1.3 mu M). In similar experiments, the calculated, IC50 values for other antioxidants compared are 1.5 +/- 0.05 mu M (carnosol), 2.25 +/- 0.08 mu M (carnosic acid), 65 +/- 2.6 mu M (Trolox C), and 250 +/- 10 mu M (vitamin E). Hydroxytyrosol and ascorbate reduced copper(II) ions to their copper(I) prooxidant form, but this was not reflected by their abilities to induce oxidative DNA damage in the complex copper-phenanthroline. Only high, nonphysiological, millimolar concentrations of pure hydroxytyrosol weakly stimulated copper-dependent chemical modification to DNA bases. The prooxidant (redox actions on metal ions) concentrations in vitro may never be achieved in vivo (following consumption of extra virgin olive oil). Thus, hydroxytyrosol may represent a useful diet-derived antioxidant depending on its bioavailability.
引用
收藏
页码:5181 / 5187
页数:7
相关论文
共 50 条
[11]  
ARUOMA OI, 1999, ASIA PACIFIC J CLIN, V8
[12]  
BARALDI PG, 1983, LIEBIGS ANN CHEM, P684
[13]  
Braga C, 1998, CANCER-AM CANCER SOC, V82, P448, DOI 10.1002/(SICI)1097-0142(19980201)82:3&lt
[14]  
448::AID-CNCR4&gt
[15]  
3.0.CO
[16]  
2-L
[17]  
Cadet J, 1997, Rev Physiol Biochem Pharmacol, V131, P1
[18]  
COK NC, 1996, NUTR BIOCH, V7, P66
[19]   CHEMICAL DETERMINATION OF FREE RADICAL-INDUCED DAMAGE TO DNA [J].
DIZDAROGLU, M .
FREE RADICAL BIOLOGY AND MEDICINE, 1991, 10 (3-4) :225-242
[20]   MODIFICATION OF BASES IN DNA BY COPPER ION-1,10-PHENANTHROLINE COMPLEXES [J].
DIZDAROGLU, M ;
ARUOMA, OI ;
HALLIWELL, B .
BIOCHEMISTRY, 1990, 29 (36) :8447-8451