Cytotoxic effects of zearalenone and its metabolites and antioxidant cell defense in CHO-K1 cells.

6533b854fe1ef96bd12af3eb

RESEARCH PRODUCT

Cytotoxic effects of zearalenone and its metabolites and antioxidant cell defense in CHO-K1 cells.

Guillermina Font Elena Tatay María-josé Ruiz

subject

0301 basic medicine Antioxidant DNA damage medicine.medical_treatment Immunoblotting CHO Cells Toxicology Antioxidants Superoxide dismutase 03 medical and health sciences chemistry.chemical_compound Cricetulus Cricetinae medicine Animals Estrogens Non-Steroidal Cell damage chemistry.chemical_classification Reactive oxygen species Glutathione Peroxidase biology Superoxide Dismutase Glutathione peroxidase food and beverages General Medicine Glutathione medicine.disease Catalase Glutathione Comet assay 030104 developmental biology chemistry Biochemistry biology.protein Zearalenone Zeranol Comet Assay Reactive Oxygen Species Oxidation-Reduction Food Science DNA Damage

description

Zearalenone (ZEA) and its metabolites (α-zearalenol; α-ZOL, β-zearalenol; β-ZOL) are secondary metabolites of Fusarium fungi that produce cell injury. The present study explores mycotoxin-induced cell damage and cellular protection mechanisms in CHO-K1 cells. Cytotoxicity has been determined by reactive oxygen species (ROS) production and DNA damage. ROS production was determined using the fluorescein assay and DNA strand breakage by comet assay. Intracellular protection systems were glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD). The results demonstrated that all mycotoxins increased the ROS levels up to 5.3-fold the control levels in CHO-K1 cells. Zearalenone metabolites, but not ZEA, increased DNA damage 43% (α-ZOL) and 28% (β-ZOL) compared to control cells. The GSH levels decreased from 18% to 36%. The GPx and SOD activities respectively increased from 26% to 62% and from 23% to 69% in CHO-K1 cells, whereas CAT activity decreased from 14% to 52%. In addition, intracellular ROS production was induced by ZEA and its metabolites. The endogenous antioxidant system components GSH, GPx and SOD were activated against ZEA and its metabolites. These antioxidant system components thus could contribute to decrease cell injury by ZEA and its metabolites.

year	journal	country	edition	language
2016-06-08	Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

10.1016/j.fct.2016.07.027 https://pubmed.ncbi.nlm.nih.gov/27465603