Alleviation of aflatoxin B1-induced oxidative stress in HepG2 cells by volatile extract from Allii Fistulosi Bulbus

被引:29
作者
Lee, JK
Choi, EH
Lee, KG
Chun, HS
机构
[1] Korea Food Res Inst, Food Funct Res Div, Sungnam 463746, South Korea
[2] Dongguk Univ, Dept Food Sci & Technol, Seoul 100715, South Korea
关键词
volatile extract from the Allii Fistulosi Bulbus (VEA-F); aflatoxin B-1; oxidative stress; 8-hydroxy-2 '-deoxyguanosine; metabolizing enzymes;
D O I
10.1016/j.lfs.2005.03.028
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The volatile extract from Allii Fistulosi Bulbus (VEAF) was isolated by steam distillation under reduced pressure, followed by continuous liquid-liquid extraction, and its effects on aflatoxin B-1 (AFB(1))-induced oxidative stress were investigated in human hepatoma cells (HepG2). The main constituents of the VEAF, identified by gas chromatography/mass spectrometry, were 2-octyl-5-methyl-3(2H)-furanone, 2-hexyl-5-methyl-3(2H)-furanone, 2,5-dimethylthiophene, 3,5-diethyl-1,2,4-trithiolane and 3,4-dimethyl-2,5-dihydro-thiophene-2-one. VEAF significantly inhibited the formation of intracellular reactive oxygen species caused by AFB(1) in a dose-dependent manner, concomitant with a significant decrease in the AFB(1)-induced cytotoxicity. VEAF pretreatment significantly reduced the levels of thiobarbituric acid reactive substances, an indicator of lipid peroxidation, whereas increased the level of reduced glutathione. The level of 8-hydroxy-2'-deoxyguanosine, a DNA oxidative stress marker, was also decreased by 49-59% with pretreatment of VEAF. With respect to the activity of AFB(1) metabolizing enzymes, VEAF significantly increased the activity of glutathione S-transferase, and significantly decreased the cytochrome (CYP) P450 3A4 activity, but had a little effect on the CYP1As. These results suggest that VEAF may be selectively effective in alleviating the AFB I -induced oxidative stress, and lead to cytoprotection against AFB(1) exposure. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:2896 / 2910
页数:15
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