Naslov
Induction of reactive oxygen species by fumonisin B1

Autori
Domijan, Ana-Marija ; Abramov, Andrey Y.

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
COST Workshop CM0603 Free Radicals in Chemical Biology / Mihaljević, Branka - Zagreb : Institut Ruđer Bošković, 2011, 58-58

ISBN
978-953-6690-88-6

Skup
COST Workshop CM0603 - Free Radicals in Chemical Biology

Mjesto i datum
Zagreb, Hrvatska, 14.06.2011. - 17.06.2011

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
fumonisin B1; mycotoxins; reactive oxygen species; live imaging

Sažetak
Fumonisin B1 (FB1) is a mycotoxin, secondary metabolite of Fusarium verticiloides mould that contaminates maize world-wide. It is toxic to domestic and experimental animals and some human diseases as oesophageal cancer, primary liver cancer and neural tube defect were connected to exposure to FB1. The mechanism of FB1 toxicity is not completely understood. Since FB1 chemical structure is similar to sphingoid bases, FB1 toxicity has been connected with deregulation of sphingolipid metabolism. Also, oxidative stress was proposed to be involved in FB1 toxicity. The aim of this study was to explore mechanism and sources of reactive oxygen species (ROS) production upon FB1 exposure (0.5 µM, 5 µM and 50 µM) on human neuroblastoma (SH-SY5Y) cells. Dihydroethidium (HEt) an indicator of production of ROS (mostly superoxide) in cytosol and MitoSOX an indicator of ROS production in mitochondria were used. ROS production was monitored on epifluorescence inverted microscope ; all imaging data were collected and analysed using software from Andor, and statistical difference of results were tested using Statistica 8.0 program. FB1 significantly increased the rate of ROS production already with lowest dose (124.9±5.0 ; n=4 experiments, p<0.05), but the effect was not dose-dependent. Inhibition of NADPH oxidase with diphenylene iodonium (DPI) and inhibition of glutathione with monochlorobiamine (MCB) had no effect on the ability of FB1 to increase the rate of ROS production. However, the uncoupler of the mitochondrial respiratory chain, carbonyl cyanide p-trifluoromethoxy-phenylhydrazone (FCCP) completely blocked the ROS production stimulated with FB1. The rate of ROS production after inhibition with FCCP was even lower compared to the basic rate of ROS in control cells from 81.7±2.8 for 0.5 µM to 77.0±5.4 for 50µM concentration (n=4 experiments ; p<0.05). In MitoSOX experiments, all doses of FB1 increased MitoSOX florescence, but only the lowest concentration had significant effect (125.3±3.2% ; n=3 experiments ; p<0.05). Taken together our results suggest a mitochondrial origin of FB1-induced ROS production and point to a specific role of the mitochondrial respiratory chain in FB1 response.

Izvorni jezik
Engleski

Znanstvena područja
Biologija, Temeljne medicinske znanosti, Javno zdravstvo i zdravstvena zaštita

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