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  • Nuclear factor-κB inhibitors alleviate nivalenol-induced cytotoxicity in HL60 cells.

Nuclear factor-κB inhibitors alleviate nivalenol-induced cytotoxicity in HL60 cells.

Environmental toxicology and pharmacology (2011-07-27)
Hitoshi Nagashima, Masayo Kushiro, Hiroyuki Nakagawa
ABSTRACT

Tricothecene mycotoxins, such as nivalenol, are toxic to leukocytes. To elucidate the molecular mechanism of nivalenol toxicity, we investigated the involvement of nuclear factor-κB (NF-κB) in nivalenol-induced cytotoxicity in HL60 cells using the NF-κB inhibitors pyrrolidinedithiocarbamate (PDTC) and dexamethasone. Cells were treated with the chemicals for 24h before assays were performed. Nivalenol elicited interleukin (IL)-8 secretion. IL-8 secretion was lower in cells concomitantly treated with nivalenol and NF-κB 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-κB inhibitors than with nivalenol alone. NF-κB inhibitors thus alleviated the effects of nivalenol, indicating that NF-κB is important for nivalenol-caused changes in cytokine secretion. Nivalenol hindered cell proliferation, and dexamethasone reduced this effect, suggesting that NF-κB contributes to cell proliferation. Thus, it appears that NF-κB is involved in nivalenol-induced toxicity in HL60 cells.

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Supelco
Nivalenol solution, 100 μg/mL in acetonitrile, analytical standard
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Nivalenol in acetonitrile, IRMM®, certified reference material
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