In vitro evaluation of the chemoprotective action mechanisms of leontopodic acid against aflatoxin B1 and deoxynivalenol-induced cell damage

被引:39
|
作者
Costa, Stefano [1 ]
Schwaiger, Stefan [2 ]
Cervellati, Rinaldo [3 ]
Stuppner, Hermann [1 ]
Speroni, Ester [1 ]
Guerra, Maria Clelia [1 ]
机构
[1] Univ Bologna, Dept Pharmacol, I-40126 Bologna, Italy
[2] Univ Innsbruck, Inst Pharm Pharmacognosy, CMBI, A-6020 Innsbruck, Austria
[3] Univ Bologna, Dept Chem G Ciamician, I-40126 Bologna, Italy
关键词
antioxidants; chemoprotection; detoxifying enzymes; glutathione; mycotoxins; LIPID-PEROXIDATION; MYCOTOXINS; B-1; TOXICOLOGY;
D O I
10.1002/jat.1372
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Several in vitro studies showed that free radical scavengers possess chemopreventive properties against mycotoxin-induced cell damage which are at least partially associated with the induction of phase 11 detoxifying enzymes and antioxidant enzymes like glutathione S-transferase (GST) and glutathione peroxidase (GPx). The aim of this project was to study the chemopreventive effects of leontopodic acid (LA), a potent natural occurring free radical scavenger isolated from the aerial parts of Leontopodium alpinum. Different mycotoxins were evaluated in two different cell lines on the basis of their specific toxicity: aflatoxin B1 (AFB1) on HepG2 cells and deoxynivalenol (DON) on U937 cells. Cell viability and reactive oxygen species concentration were determined, and the effects of pre-treatment with LA on these parameters were investigated together with the GST and GPx activity as well as the concentration of reduced glutathione. The results show that LA protects U937 cells from DON-induced cell damage but not HepG2 cells from AFB1. Moreover LA is able to enhance GPx activity in U937, but not GST activity in HepG2. We hypothesize that the increase in detoxifying enzymes is probably the main mechanism of antioxidant mediated chemoprevention. Copyright (C) 2008 John Wiley & Sons, Ltd.
引用
收藏
页码:7 / 14
页数:8
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