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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Lee, Hyungkyoung Kang, Changgeun Yoo, Yong-San Hah, Do-Yun Kim, Chung Hui Kim, Euikyung Kim, Jong Shu |
| Description | Author Affiliation: Lee H ( Department of Pharmacology & Toxicology, College of Veterinary Medicine, Gyeongsang National University, Jinju Dae-lo 501, Jinju 660-701, Republic of Korea.) |
| Abstract | Zearalenone (ZEN) has been implicated in several cases of mycotoxicosis in farm animals and humans. The toxic effects of ZEN have been well characterized, but little is known regarding the mechanisms of ZEN toxicity, including the involvement of the oxidative stress pathway. Using Chang liver cells as a model, the aim of this study was to determine if ZEN could elevate the expression of the heat shock protein Hsp 70, induce cytotoxicity and modulate the levels of glutathione (GSH) and thiobarbituric acid reactive substance (TBARS). In addition, the cytoprotective effects of N-acetylcysteine amide (NACA) pre-treatment were assessed. Finally, the involvement of oxidative stress in ZEN-induced toxicity was confirmed. The results of this study demonstrated that ZEN-induced Hsp 70 expression in a dose- and time-dependent manners. This effect occurred at low-ZEN concentrations, and could therefore be considered a biomarker of ZEN-induced toxicity. The cytotoxicity was reduced when Chang liver cells were exposed to sub-lethal heat shock prior to ZEN treatment, demonstrating a cytoprotective effect of Hsp 70. This cytoprotective effect suggested that Hsp 70 might play a key role in the cellular defense mechanism. When cells were pre-treated with NACA prior to ZEN treatment, the cells were also protected from toxicity. This NACA cytoprotective effect suggested the involvement of oxidative stress in ZEN-induced toxicity, and this mechanism was supported by reduced Hsp 70 expression, inhibited cytolethality, increased GSH levels and decreased TBARS formation when cells were pre-treated with NACA prior to ZEN exposure. Our data clearly demonstrated that ZEN induced cytotoxicity in Chang liver cells by inhibiting cell proliferation, decreasing GSH levels and increasing TBARS formation in a dose-dependent manner. ZEN also, induced Hsp 70 expression, and the side effects of ZEN were significantly alleviated by pre-treatment with NACA. Oxidative stress is likely to be one of the primary pathways of ZEN toxicity. This oxidative stress may contribute, at least in part, to the mechanism of ZEN-induced cytotoxicity. |
| File Format | HTM / HTML |
| ISSN | 13826689 |
| Issue Number | 2 |
| Volume Number | 36 |
| e-ISSN | 18727077 |
| Journal | Environmental Toxicology and Pharmacology |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2013-09-01 |
| Publisher Place | Netherlands |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Environmental Health Discipline Pharmacology Hsp70 Heat-shock Proteins Metabolism Hepatocytes Drug Effects Oxidative Stress Zearalenone Toxicity Antioxidants Pharmacology Biological Markers Cell Proliferation Cytoprotection Dose-response Relationship, Drug Glutathione Hep G2 Cells Pathology Humans Thiobarbituric Acid Reactive Substances Time Factors Up-regulation Journal Article |
| Content Type | Text |
| Resource Type | Article |
| Subject | Health, Toxicology and Mutagenesis Medicine Toxicology Pharmacology |
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