Exposure of human lymphoma cells (U-937) to the action of a single mycotoxin as well as in mixtures with the potential protectors 24-epibrassinolide and selenium ions

被引:3
作者
Barbasz, Anna [1 ]
Rudolphi-Skorska, Elzbieta [1 ]
Filek, Maria [1 ,2 ]
Janeczko, Anna [2 ]
机构
[1] Pedag Univ Cracow, Inst Biol, Podchorazych 2, PL-30084 Krakow, Poland
[2] Polish Acad Sci, Inst Plant Physiol, Podluzna 3, PL-30239 Krakow, Poland
关键词
Zearalenone; Mycotoxin; Human cells; Monocytes; Membranes; Langmuir monolayers; U-937; OXIDATIVE STRESS; INDUCED CYTOTOXICITY; DNA-DAMAGE; ZEARALENONE; AFLATOXIN; TOXICITY; METABOLITES; OCHRATOXIN; INDUCTION; APOPTOSIS;
D O I
10.1007/s12550-018-0334-1
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The progressive contamination of food products by mycotoxins such as zearalenone (ZEN) has prompted the search for specific substances that can act as protectors against an accumulation of these toxins. This paper discusses the effect of selenium ions and 24-epibrassinolide (EBR) as non-organic and organic compounds that preserve human lymphoblastic cells U-937 under ZEN stressogenic conditions. Based on measurements of cell viability and a DAPI test, concentrations of ZEN at 30mol/l, Se at 2.5mol/l and EBR at 0.005mol/l were selected. The addition of both protectors resulted in an increase in the viability of ZEN-treated cells by about 16%. This effect was connected with a decrease in lipid peroxidation (a decrease in the malonyldialdehyde content) and the generation of reactive oxygen species, which were determined by a cellular ROS/superoxide detection assay and the SOD activity. The Se protection was observed as the blocking of the all excess ROS, while the EBR action was mainly concentrated on something other than the superoxide radical itself. The experiments on the model lipid membranes that mimic the environment of U-937 cells confirmed the affect of ZEN on the structure and physicochemical properties of human membranes. Although the presence of both Se and EBR reduced the effect of ZEN by blocking its interaction with a membrane, the action of Se was more evident.
引用
收藏
页码:89 / 98
页数:10
相关论文
共 47 条
[31]   Mycotoxins - Contemporary issues of food animal health and productivity [J].
Osweiler, GD .
VETERINARY CLINICS OF NORTH AMERICA-FOOD ANIMAL PRACTICE, 2000, 16 (03) :511-+
[32]   Induction of micronuclei by Zearalenone in Vero monkey kidney cells and in bone marrow cells of mice: protective effect of Vitamin E [J].
Ouanes, Z ;
Abid, S ;
Ayed, I ;
Anane, R ;
Mobio, T ;
Creppy, EE ;
Bacha, H .
MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS, 2003, 538 (1-2) :63-70
[33]   Lipid peroxidation-mediated cytotoxicity and DNA damage in U937 cells [J].
Park, JE ;
Yang, JH ;
Yoon, SJ ;
Lee, JH ;
Yang, ES ;
Park, JW .
BIOCHIMIE, 2002, 84 (12) :1199-1205
[34]   The importance of selenium to human health [J].
Rayman, MP .
LANCET, 2000, 356 (9225) :233-241
[35]   Impact of polyphenol-rich green tea extracts on the protection of DOPC monolayer against damage caused by ozone induced lipid oxidation [J].
Rudolphi-Skorska, Elzbieta ;
Dyba, Barbara ;
Kreczmer, Barbara ;
Filek, Maria .
ACTA BIOCHIMICA POLONICA, 2018, 65 (02) :193-197
[36]   The Effects of the Structure and Composition of the Hydrophobic Parts of Phosphatidylcholine-Containing Systems on Phosphatidylcholine Oxidation by Ozone [J].
Rudolphi-Skorska, Elzbieta ;
Filek, Maria ;
Zembala, Maria .
JOURNAL OF MEMBRANE BIOLOGY, 2017, 250 (05) :493-505
[37]   α-Tocopherol/Gallic Acid Cooperation in the Protection of Galactolipids Against Ozone-Induced Oxidation [J].
Rudolphi-Skorska, Elzbieta ;
Filek, Maria ;
Zembala, Maria .
JOURNAL OF MEMBRANE BIOLOGY, 2016, 249 (1-2) :87-95
[38]   INVOLVEMENT OF SELENIUM IN PROTECTIVE MECHANISMS OF PLANTS UNDER ENVIRONMENTAL STRESS CONDITIONS - REVIEW [J].
Sieprawska, Apolonia ;
Kornas, Andrzej ;
Filek, Maria .
ACTA BIOLOGICA CRACOVIENSIA SERIES BOTANICA, 2015, 57 (01) :9-20
[39]  
Spyrou G, 1996, CANCER RES, V56, P4407
[40]   Induction of differentiation and apoptosis by sodium selenite in human colonic carcinoma cells (HT29) [J].
Stewart, MS ;
Davis, RL ;
Walsh, LP ;
Pence, BC .
CANCER LETTERS, 1997, 117 (01) :35-40