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Article

Oxygen Consumption Rate Analysis of Mitochondrial Dysfunction Caused by Bacillus cereus Cereulide in Caco-2 and HepG2 Cells

1
Department of Food Technology, Food Safety and Health, Faculty of Bioscience Engineering, Ghent University, Coupure Links 653, 9000 Ghent, Belgium
2
Laboratory of Food Analysis, Department of Bioanalysis, Faculty of Pharmaceutical Sciences, Ghent University, Ottergemsesteenweg 460, 9000 Ghent, Belgium
3
Department of Food Preservation Engineering, Faculty of Technology, University of Novi Sad, Bulevar Cara Lazara 1, 21000 Novi Sad, Serbia
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Department of Food Safety and Food Quality Management, Faculty of Agriculture, University of Belgrade, Nemanjina 6, 11081 Zemun-Belgrade, Serbia
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Department of Organic and Macromolecular Chemistry, Organic and Biomimetic Chemistry Research Group, Faculty of Sciences, Campus Sterre, Krijgslaan 281, Building S4, 9000 Gent, Belgium
*
Author to whom correspondence should be addressed.
Received: 8 June 2018 / Revised: 20 June 2018 / Accepted: 22 June 2018 / Published: 2 July 2018
(This article belongs to the Collection Bacterial Enterotoxins)
The emetic syndrome of Bacillus cereus is a food intoxication caused by cereulide (CER) and manifested by emesis, nausea and in most severe cases with liver failure. While acute effects have been studied in the aftermath of food intoxication, an exposure to low doses of cereulide might cause unnoticed damages to the intestines and liver. The toxicity which relies on the mitochondrial dysfunction was assessed on Caco-2 and HepG2 cells after exposure of one, three and ten days to a range of low doses of cereulide. Oxygen consumption rate analyses were used to study the impact of low doses of CER on the bioenergetics functions of undifferentiated Caco-2 and HepG2 cells using Seahorse XF extracellular flux analyzer. Both Caco-2 and HepG2 cells experienced measurable mitochondrial impairment after prolonged exposure of 10 days to 0.25 nM of cereulide. Observed mitochondrial dysfunction was greatly reflected in reduction of maximal cell respiration. At 0.50 nM CER, mitochondrial respiration was almost completely shut down, especially in HepG2 cells. These results corresponded with a severe reduction in the amount of cells and an altered morphology, observed by microscopic examination of the cells. Accurate and robust quantification of basal respiration, ATP production, proton leak, maximal respiration, spare respiratory capacity, and non-mitochondrial respiration allowed better understanding of the effects of cereulide in underlying respiratory malfunctions in low-dose exposure. View Full-Text
Keywords: cereulide; emetic toxin; Bacillus cereus; Seahorse XF; extracellular flux; mitochondrial dysfunction; respiration; oxygen consumption rate; depsipeptides cereulide; emetic toxin; Bacillus cereus; Seahorse XF; extracellular flux; mitochondrial dysfunction; respiration; oxygen consumption rate; depsipeptides
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MDPI and ACS Style

Decleer, M.; Jovanovic, J.; Vakula, A.; Udovicki, B.; Agoua, R.-S.E.K.; Madder, A.; De Saeger, S.; Rajkovic, A. Oxygen Consumption Rate Analysis of Mitochondrial Dysfunction Caused by Bacillus cereus Cereulide in Caco-2 and HepG2 Cells. Toxins 2018, 10, 266. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins10070266

AMA Style

Decleer M, Jovanovic J, Vakula A, Udovicki B, Agoua R-SEK, Madder A, De Saeger S, Rajkovic A. Oxygen Consumption Rate Analysis of Mitochondrial Dysfunction Caused by Bacillus cereus Cereulide in Caco-2 and HepG2 Cells. Toxins. 2018; 10(7):266. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins10070266

Chicago/Turabian Style

Decleer, Marlies, Jelena Jovanovic, Anita Vakula, Bozidar Udovicki, Rock-Seth E.K. Agoua, Annemieke Madder, Sarah De Saeger, and Andreja Rajkovic. 2018. "Oxygen Consumption Rate Analysis of Mitochondrial Dysfunction Caused by Bacillus cereus Cereulide in Caco-2 and HepG2 Cells" Toxins 10, no. 7: 266. https://0-doi-org.brum.beds.ac.uk/10.3390/toxins10070266

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