Abstract

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(2 H)-furanone, 2-hexyl-5-methyl-3(2 H)-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 1-induced oxidative stress, and lead to cytoprotection against AFB 1 exposure.

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