Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8324969 | The International Journal of Biochemistry & Cell Biology | 2011 | 8 Pages |
Abstract
Fumonisin B1 (FB1) is a neurodegenerative mycotoxin produced by Fusarium verticiloides mould that contaminates maize worldwide. FB1 toxicity has been connected with deregulation of sphingolipid metabolism, but the mechanism of cytotoxicity remains controversial. In cell cultures of rat primary astrocytes and human neuroblastoma (SH-SY5Y), we found that FB1 inhibits mitochondrial complex I, which leads to a decrease in the rate of mitochondrial and cellular respiration, depolarisation of the mitochondrial membrane, induction of reactive oxygen species (ROS) production in mitochondria and deregulation of calcium signalling. Despite the increase in ROS production, the intracellular level of glutathione (GSH) was significantly increased. After 24Â h of FB1 exposure, no cell death was observed. Thus, mitochondria appear to be the primary target of FB1, which leads to sustained deregulation of calcium homeostasis and presumably to cell death.
Keywords
MPTPcarbonyl cyanide p-trifluoromethoxy-phenylhydrazoneRh123MrOSMCBCrosΔΨmFCCPDPIFB1GSHHETmitochondrial ROS[Ca2+]cIARC یا International Agency for Research on CancerInternational Agency for Research on Cancermitochondrial permeability transition poredihydroethidiumdiphenylene iodoniumRhodamine 123NeurotoxicityCa2+ signallingFumonisin B1MycotoxinsMitochondriaMitochondrial membrane potentialPropidium iodideGlutathioneReactive oxygen species
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Authors
Ana-Marija Domijan, Andrey Y. Abramov,