PDF(Pubmed)
Abstract：
This study investigates the genotoxicity and cytotoxicity of C17-sphinganine analog mycotoxin (C17-SAMT) using in vitro assays. C17-SAMT was previously identified as the cause of unusual toxicity in cultured mussels from the Bizerte Lagoon in northern Tunisia. While a previous in vivo genotoxicity study was inconclusive, in vitro results demonstrated that C17-SAMT induced an increase in micronucleus formation in human lymphoblastoid TK6 cells at concentrations of 0.87 µM and 1.74 µM. In addition, multiparametric cytotoxicity assays were performed in the human hepatoma HepaRG cell line, which showed that C17-SAMT induced mitochondrial dysfunction, decreased cellular ATP levels, and altered the expression of various proteins, including superoxide dismutase SOD2, heme oxygenase HO-1, and NF-κB. These results suggest that C17-SAMT is mutagenic in vitro and can induce mitochondrial dysfunction in HepaRG cells. However, the exact mode of action of this toxin requires further investigation. Overall, this study highlights the potential toxicity of C17-SAMT and the need for further research to better understand its effects.
摘要：
本研究使用体外测定法研究了C17-鞘氨醇类似物霉菌毒素（C17-SAMT）的遗传毒性和细胞毒性。C17-SAMT先前被确定为突尼斯北部比泽特泻湖养殖贻贝异常毒性的原因。虽然先前的体内遗传毒性研究尚无定论，体外结果表明，在0.87µM和1.74µM的浓度下，C17-SAMT诱导了人类淋巴母细胞TK6细胞微核形成的增加。此外,在人肝癌HepaRG细胞系中进行多参数细胞毒性测定，这表明C17-SAMT诱导线粒体功能障碍，细胞ATP水平降低，改变了各种蛋白质的表达，包括超氧化物歧化酶SOD2、血红素加氧酶HO-1和NF-κB。这些结果表明，C17-SAMT在体外具有致突变性，并且可以诱导HepaRG细胞的线粒体功能障碍。然而,这种毒素的确切作用方式需要进一步研究。总的来说,本研究强调了C17-SAMT的潜在毒性以及进一步研究以更好地了解其作用的必要性.
