Lactoferrin inhibits aflatoxin B1-and aflatoxin M1-induced cytotoxicity and DNA damage in Caco-2, HEK, Hep-G2, and SK-N-SH cells

文献类型： 外文期刊

第一作者： Zheng, Nan

作者： Zheng, Nan;Li, Songli;Wang, Jiaqi;Gao, Yanan;Zheng, Nan;Li, Songli;Wang, Jiaqi;Gao, Yanan;Zheng, Nan;Li, Songli;Wang, Jiaqi;Gao, Yanan;Zheng, Nan;Li, Songli;Wang, Jiaqi;Gao, Yanan;Zhang, Huan;Ren, Hui;Liu, Jia

作者机构：

关键词： Aflatoxins; Lactoferrin; Oxidative DNA damage; MAPK pathway

期刊名称：TOXICON （ 影响因子：3.033； 五年影响因子：2.689 ）

ISSN： 0041-0101

年卷期： 2018 年 150 卷

页码：

收录情况： SCI

摘要： Aflatoxins, including aflatoxin B-1 (AFB(1)) and M-1 (AFM(1)), are natural potent carcinogens produced by Aspergillus spp. These compounds, which can often be detected in dairy foods, can cause diseases in human beings. However, the molecular mechanisms involved in cytotoxicity, as well as methods for intervention, remain largely unexplored. For example, it is unclear whether lactoferrin (LF), a major antioxidant in milk, can inhibit the cytotoxicity of AFB(1) and AFM(1). In this study, we assessed AFB(1)- and AFM(1)-induced cell toxicity by measuring cell viability, membrane permeability, and genotoxicity, and then investigated the ability of LF to protect cells against AFB(1) and AFM(1). In Caco-2, HEK, Hep-G2, and SK-N-SH cells, 4 mu g/mL AFB(1) or AFM(1) significantly inhibited cell growth, increased the level of lactate dehydrogenase, induced genetic damage, and increased the levels of signal-regulated kinase (ERK1/2) and c-Jun N-terminal kinase (JNK) (p < 0.05). AFBi was more genotoxic than AFM(1) in all four cell lines, especially in Hep-G2. In Caco-2, Hep-G2, and SK-N-SH, incubation of AF-treated cells with 1000 mu g/mL LF significantly decreased cytotoxicity, oxidation level, DNA damage, and levels of ERK1/2 and JNK (p < 0.05). Our data demonstrate that AFBi or AFM(1) induced cytotoxicity and DNA damage in these four cell lines, and that LF alleviated toxicity by decreasing oxidative stress mediated by mitogen-activated protein kinase pathways. (C) 2018 Elsevier Ltd. All rights reserved.

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