Fumonisin B₁-induced apoptosis in neuroblastoma, glioblastoma and hypothalamic cell lines

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• 作者：Helene Stockmann-Juvala ; Jonne Naarala ; Jarkko Loikkanen ; Kirsi Vä ; hä ; kangas and Kai Savolainen
• 关键词：Fumonisin B₁ ; Apoptosis ; Neurotoxicity ; Caspase-3 ; Bcl-2 ; p53
• 刊名：Toxicology
• 出版年：2006
• 出版时间：15 August 2006
• 年：2006
• 卷：225
• 期：2-3
• 页码：234-241
• 全文大小：222 K

文摘

Fumonisin B₁ (FB₁) is a mycotoxin produced by Fusarium verticilliodes, which commonly infects corn across the world. Fusarium fungi may also be found in moisture-damaged buildings. In this study, we investigated the role of apoptosis in the toxicity of FB₁ in four different cell lines. Activation of caspase-3-like protease, DNA fragmentation and expression of p53 and Bcl-2 family proteins were studied in mouse GT1-7 hypothalamic, rat C6 glioblastoma, human U-118MG glioblastoma, and human SH-SY5Y neuroblastoma cells exposed to 0.1–100 μM FB₁ for 0–144 h. Caspase-3-like protease activity increased in all cell lines, except SH-SY5Y, at 48–144 h, and internucleosomal DNA fragmentation occurred in all of the cell lines, pointing to a role for apoptosis in the toxicity of FB₁. However, the expressions of p53 or pro- or antiapoptotic Bcl-2 family proteins (Bax, Bcl-2, Bcl-X_L and Mcl-1) were not affected in any of the cell lines even after prolonged exposure to FB₁ at high doses. The results of this study, together with the results of our previous studies, provide evidence that FB₁ is a potential neurotoxin, but that the toxicity of FB₁ varies between different cell lines. The sensitivity of these cell lines towards FB₁ is as follows: U-118MG > GT1-7 > C6 > SH-SY5Y cells. These results are consistent with the assumption that cells of glial origin may be more sensitive towards FB₁ than cells of neural origin.