RRC ID 17656
Author Nagashima H, Kushiro M, Nakagawa H.
Title Nuclear factor-κB inhibitors alleviate nivalenol-induced cytotoxicity in HL60 cells.
Journal Environ Toxicol Pharmacol
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.
Volume 31(1)
Pages 258-61
Published 2011-1
DOI 10.1016/j.etap.2010.09.014
PII S1382-6689(10)00171-7
PMID 21787693
MeSH Anti-Inflammatory Agents / pharmacology Antioxidants / pharmacology Cell Proliferation / drug effects Cell Survival / drug effects Chemokine CCL2 / metabolism Cytokines / metabolism Dexamethasone / pharmacology HL-60 Cells Humans Interleukin-8 / metabolism Mycotoxins / antagonists & inhibitors* Mycotoxins / toxicity NF-kappa B / antagonists & inhibitors NF-kappa B / physiology* Proline / analogs & derivatives Proline / pharmacology Thiocarbamates / pharmacology Trichothecenes / antagonists & inhibitors* Trichothecenes / toxicity*
IF 3.061
Times Cited 7
Human and Animal Cells HL60 (RCB0041)