期刊
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
卷 31, 期 1, 页码 258-261出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.etap.2010.09.014
关键词
Dexamethasone; Interleukin-8; Monocyte chemotactic protein-1; Nivalenol; Nuclear factor-kappa B; Pyrrolidinedithiocarbamate
资金
- Ministry of Agriculture, Forestry, and Fisheries of Japan [MT-3115]
Tricothecene mycotoxins, such as nivalenol, are toxic to leukocytes. To elucidate the molecular mechanism of nivalenol toxicity, we investigated the involvement of nuclear factor-kappa B (NF-kappa B) in nivalenol-induced cytotoxicity in HL60 cells using the NF-kappa B inhibitors pyrrolidinedithiocarbamate (PDTC) and dexamethasone. Cells were treated with the chemicals for 24 h before assays were performed. Nivalenol elicited interleukin (IL)-8 secretion. IL-8 secretion was lower in cells concomitantly treated with nivalenol and NF-kappa B inhibitors than with nivalenol alone. Nivalenol reduced monocyte chemotactic protein (MCP)-1 secretion. MCP-1 secretion was higher in cells concomitantly treated with nivalenol and NF-kappa B inhibitors than with nivalenol alone. NF-kappa B inhibitors thus alleviated the effects of nivalenol, indicating that NF-kappa B is important for nivalenol-caused changes in cytokine secretion. Nivalenol hindered cell proliferation, and dexamethasone reduced this effect, suggesting that NF-kappa B contributes to cell proliferation. Thus, it appears that NF-kappa B is involved in nivalenol-induced toxicity in HL60 cells. (C) 2010 Elsevier B.V. All rights reserved.
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