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Article

Bioenergetic Status of the Intestinal and Hepatic Cells after Short Term Exposure to Fumonisin B1 and Aflatoxin B1

1
Department of Food Technology, Safety and Health, Faculty of Bioscience Engineering, Ghent University, 9000 Ghent, Belgium
2
Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, Assiut University, Assiut 71515, Egypt
*
Author to whom correspondence should be addressed.
Academic Editor: Soo-Jin Choi
Int. J. Mol. Sci. 2022, 23(13), 6945; https://doi.org/10.3390/ijms23136945
Received: 23 March 2022 / Revised: 20 June 2022 / Accepted: 21 June 2022 / Published: 22 June 2022
(This article belongs to the Special Issue Food Toxicants 2.0)
Fumonisin B1 (FB1) and aflatoxin B1 (AFB1) are frequent contaminants of staple foods such as maize. Oral exposure to these toxins poses health hazards by disrupting cellular signaling. However, little is known regarding the multifaced mitochondrial dysfunction-linked toxicity of FB1 and AFB1. Here, we show that after exposure to FB1 and AFB1, mitochondrial respiration significantly decreased by measuring the oxygen consumption rate (OCR), mitochondrial membrane potential (MMP) and reactive oxygen species (ROS). The current work shows that the integrity of mitochondria (MMP and ROS), that is the central component of cell apoptosis, is disrupted by FB1 and AFB1 in undifferentiated Caco-2 and HepG2 cells as in vitro models for human intestine and liver, respectively. It hypothesizes that FB1 and AFB1 could disrupt the mitochondrial electron transport chain (ETC) to induce mitochondrial dysfunction and break the balance of transferring H+ between the mitochondrial inner membrane and mitochondrial matrix, however, the proton leak is not increasing and, as a result, ATP synthesis is blocked. At the sub-toxic exposure of 1.0 µg/mL for 24 h, i.e., a viability of 95% in Caco-2 and HepG2 cells, the mitochondrial respiration was, however, stimulated. This suggests that the treated cells could reserve energy for mitochondrial respiration with the exposure of FB1 and AFB1, which could be a survival advantage. View Full-Text
Keywords: fumonisin B1; aflatoxin B1; cytotoxicity; mitochondrial toxicity fumonisin B1; aflatoxin B1; cytotoxicity; mitochondrial toxicity
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MDPI and ACS Style

Chen, X.; Abdallah, M.F.; Grootaert, C.; Rajkovic, A. Bioenergetic Status of the Intestinal and Hepatic Cells after Short Term Exposure to Fumonisin B1 and Aflatoxin B1. Int. J. Mol. Sci. 2022, 23, 6945. https://doi.org/10.3390/ijms23136945

AMA Style

Chen X, Abdallah MF, Grootaert C, Rajkovic A. Bioenergetic Status of the Intestinal and Hepatic Cells after Short Term Exposure to Fumonisin B1 and Aflatoxin B1. International Journal of Molecular Sciences. 2022; 23(13):6945. https://doi.org/10.3390/ijms23136945

Chicago/Turabian Style

Chen, Xiangrong, Mohamed F. Abdallah, Charlotte Grootaert, and Andreja Rajkovic. 2022. "Bioenergetic Status of the Intestinal and Hepatic Cells after Short Term Exposure to Fumonisin B1 and Aflatoxin B1" International Journal of Molecular Sciences 23, no. 13: 6945. https://doi.org/10.3390/ijms23136945

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