Aflatoxin B1 and aflatoxin M1 induced cytotoxicity and DNA damage in differentiated and undifferentiated Caco-2 cells

被引:91
作者
Zhang, J. [1 ,2 ,3 ]
Zheng, N. [1 ,3 ]
Liu, J. [4 ]
Li, F. D. [2 ]
Li, S. L. [1 ,3 ]
Wang, J. Q. [1 ,3 ]
机构
[1] Chinese Acad Agr Sci, Minist Agr, Inst Anim Sci, Lab Qual & Safety Risk Assessment Dair, Beijing 100193, Peoples R China
[2] Gansu Agr Univ, Coll Anim Sci & Technol, Lanzhou 730070, Peoples R China
[3] Chinese Acad Agr Sci, State Key Lab Anim Nutr, Inst Anim Sci, Beijing 100193, Peoples R China
[4] China Natl Res Inst Food & Fermentat Ind, Beijing 100027, Peoples R China
关键词
Aflatoxin B1; Aflatoxin M1; Caco-2; Differentiated; Cytotoxicity; DNA damage; HEP G2; OCHRATOXIN; METABOLISM; MODEL; LINE; B-1; M-1; TRANSPORT; MILK; B1;
D O I
10.1016/j.fct.2015.05.020
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Aflatoxin B1 (AFB1) and aflatoxin M1 (AFM1) are natural mycotoxins that frequently present in food and feed and pose risks to human health. There are few data in the literature regarding the impairment of them in the intestine. Therefore, the present study investigated their cytotoxic effect on Caco-2 cells, especially the differentiated ones that resemble mature small intestinal enterocytes. Both undifferentiated (UC) and differentiated (DC) cells were treated with AFB1 and AFM1 at various concentrations for up to 72 h. Cell viability, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) production and DNA damage were determined. Data showed that AFB1 and AFM1 significantly inhibited UC and DC cell growth, increased LDH and caused genetic damage in a time- and dose-dependent manner (p < 0.05). In comparison, AFB1 was found to be more toxic than AFM1 on both UC and DC. All these cytotoxic outcomes might be associated with intracellular ROS generation, leading to membrane damage and DNA strand break. Additionally, DC was found to be more sensitive to aflatoxins, which might be due to the alteration of enzymes during cell differentiation. The present study provided the first in vitro evidence of DNA damage of DC induced by AFB1 and AFM1. (C) 2015 Elsevier Ltd. All rights reserved.
引用
收藏
页码:54 / 60
页数:7
相关论文
共 31 条
[1]   Excretion of aflatoxin M1 in milk of dairy ewes treated with different doses of aflatoxin B1 [J].
Battacone, G ;
Nudda, A ;
Cannas, A ;
Borlino, AC ;
Bomboi, G ;
Pulina, G .
JOURNAL OF DAIRY SCIENCE, 2003, 86 (08) :2667-2675
[2]   Aflatoxin B1-induced DNA damage and its repair [J].
Bedard, Leanne L. ;
Massey, Thomas E. .
CANCER LETTERS, 2006, 241 (02) :174-183
[3]  
Ben Salah-Abbes J., 2014, J IMMUNOTOXICOL, V17, P1
[4]   Modulation of macrophage activity by aflatoxins B1 and B2 and their metabolites aflatoxins M1 and M2 [J].
Bianco, G. ;
Russo, R. ;
Marzocco, S. ;
Velotto, S. ;
Autore, G. ;
Severino, L. .
TOXICON, 2012, 59 (06) :644-650
[5]   Antioxidant and genoprotective effects of spent coffee extracts in human cells [J].
Bravo, Jimena ;
Arbillaga, Leire ;
Paz de Pena, M. ;
Cid, Concepcion .
FOOD AND CHEMICAL TOXICOLOGY, 2013, 60 :397-403
[6]   Oxidative base damage to DNA: specificity of base excision repair enzymes [J].
Cadet, J ;
Bourdat, AG ;
D'Ham, C ;
Duarte, V ;
Gasparutto, D ;
Romieu, A ;
Ravanat, JL .
MUTATION RESEARCH-REVIEWS IN MUTATION RESEARCH, 2000, 462 (2-3) :121-128
[7]   Aflatoxin M1 absorption and cytotoxicity on human intestinal in vitro model [J].
Caloni, F ;
Stammati, A ;
Friggè, G ;
De Angelis, I .
TOXICON, 2006, 47 (04) :409-415
[8]   A clonal cell line (BME-UV1) as a possible model to study bovine mammary epithelial metabolism: metabolism and cytotoxicity of aflatoxin B1 [J].
Caruso, M. ;
Mariotti, A. ;
Zizzadoro, C. ;
Zaghini, A. ;
Ormas, P. ;
Altafini, A. ;
Belloli, C. .
TOXICON, 2009, 53 (04) :400-408
[9]   Ochratoxin A reduces aflatoxin B1 induced DNA damage detected by the comet assay in Hep G2 cells [J].
Corcuera, L. A. ;
Arbillaga, L. ;
Vettorazzi, A. ;
Azqueta, A. ;
Lopez de Cerain, A. .
FOOD AND CHEMICAL TOXICOLOGY, 2011, 49 (11) :2883-2889
[10]   Update of survey, regulation and toxic effects of mycotoxins in Europe [J].
Creppy, EE .
TOXICOLOGY LETTERS, 2002, 127 (1-3) :19-28