Mitochondria are cellular organelles involved in many crucial functions, such as generation of energy (ATP) and initiation of apoptosis. The aim of the present study was to evaluate the role of mitochondria in the toxicity induced by sterigmatocystin (STE), a mycotoxin produced by fungi of the genus Aspergillus, on SH-SY5Y cells. Our results showed that STE exposure decreased cell viability in a time- and concentration-dependent manner by MTT assay and caused mitochondrial dysfunction, as highlighted by the increase of STE cytotoxicity in cells forced to rely on mitochondrial oxidative phosphorylation. Furthermore, intracellular ATP depletion and increased mitochondrial reactive oxygen species were also observed. Since mitochondria play a pivotal role in apoptosis, the induction of this process in response to STE exposure was decided to study. Our results showed an increase in apoptotic cell population by flow cytometry, further confirmed by the up-regulation of the expression levels of the pro-apoptotic genes Bax and Casp-3 and the down-regulation of the anti-apoptotic gene Bcl-2 by qPCR technique. Taken together, our results provide novel insights in the signalling pathways of the cell death process induced by STE in SH-SY5Y cells, highlighting the key role played by mitochondria in STE toxicity.

线粒体是参与许多关键功能的细胞器，例如能量的产生（ATP）和细胞凋亡的开始。本研究的目的是评估线粒体在由曲霉菌属真菌产生的霉菌毒素-葡萄球菌毒素（STE）诱导的毒性中的作用。在SH-SY5Y细胞上。我们的结果表明，STE暴露通过MTT分析以时间和浓度依赖性方式降低了细胞活力，并导致线粒体功能障碍，这主要是由于依赖线粒体氧化磷酸化的细胞中STE细胞毒性增加所致。此外，还观察到细胞内ATP耗竭和线粒体活性氧增加。由于线粒体在细胞凋亡中起关键作用，因此决定研究此过程对STE暴露的诱导作用。我们的结果显示，通过流式细胞仪检测凋亡细胞群的增加，进一步被促凋亡基因Bax和Casp-3的表达水平上调以及抗凋亡基因的下调进一步证实了这一点。通过qPCR技术的Bcl -2。综上所述，我们的结果为STE诱导SH-SY5Y细胞的细胞死亡过程的信号传导途径提供了新颖的见解，突出了线粒体在STE毒性中发挥的关键作用。