作者: Hitoshi Nagashima , Hiroyuki Nakagawa , Keiko Iwashita
DOI: 10.1007/978-1-4020-9646-4_46
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摘要: To elucidate the mechanism underlying toxicity of nivalenol, we investigated cytotoxicity this mycotoxin to human promyelocyte-derived cell line HL60 after 24-h exposure. Internucleosomal DNA fragmentation, a hallmark apoptosis, was apparent at 3 and 10 µg/ml nivalenol. The fragmentation these concentrations proportional morphologic damage they induced in our previous studies, indicating that apoptosis led changes morphology. In addition,1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid tetraacetoxymethyl ester (BAPTA-AM), which chelates intracellular calcium ion, considerably attenuated nivalenol-induced interleukin (IL)-8 secretion from cells, thereby induction is ion-dependent. Further, even 50 µg/ml, nivalenol failed induce mutagenesis umu test regardless treatment with S9 fraction rat liver homogenate (which rich drug-metabolizing enzymes). Therefore, unlikely be mutagenic.