
Bioenergetic status of the intestinal and hepatic cells after short term exposure to fumonisin B1 and aflatoxin B1
- Author
- Xiangrong Chen, Mohamed Fathi Abdallah (UGent) , Charlotte Grootaert (UGent) and Andreja Rajkovic (UGent)
- Organization
- Project
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- An innovative analytical platform to investigate the effect and toxicity of micro and nano plastics combined with environmental contaminants on the risk of allergic disease
- MICRO-TOX: Unravelling the in vitro toxic effects of the mycotoxin beauvericin, bacterial toxin cereulide and cyanobacterial microcystins, and their interactions with co-exposed microplastics
- Abstract
- 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 mu g/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.
- Keywords
- FUSARIUM-MYCOTOXINS, DNA-DAMAGE, HEP G2, B-1, ROS, CYTOTOXICITY, MITOCHONDRIA, EXPRESSION, APOPTOSIS, DEOXYNIVALENOL, fumonisin B1, aflatoxin B1, cytotoxicity, mitochondrial toxicity
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-8758383
- MLA
- Chen, Xiangrong, et al. “Bioenergetic Status of the Intestinal and Hepatic Cells after Short Term Exposure to Fumonisin B1 and Aflatoxin B1.” INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, vol. 23, no. 13, 2022, doi:10.3390/ijms23136945.
- APA
- Chen, X., Abdallah, M. F., Grootaert, C., & Rajkovic, A. (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(13). https://doi.org/10.3390/ijms23136945
- Chicago author-date
- Chen, Xiangrong, Mohamed Fathi 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 (13). https://doi.org/10.3390/ijms23136945.
- Chicago author-date (all authors)
- Chen, Xiangrong, Mohamed Fathi 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 (13). doi:10.3390/ijms23136945.
- Vancouver
- 1.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).
- IEEE
- [1]X. Chen, M. F. Abdallah, C. Grootaert, and A. Rajkovic, “Bioenergetic status of the intestinal and hepatic cells after short term exposure to fumonisin B1 and aflatoxin B1,” INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, vol. 23, no. 13, 2022.
@article{8758383, abstract = {{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 mu g/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.}}, articleno = {{6945}}, author = {{Chen, Xiangrong and Abdallah, Mohamed Fathi and Grootaert, Charlotte and Rajkovic, Andreja}}, issn = {{1422-0067}}, journal = {{INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES}}, keywords = {{FUSARIUM-MYCOTOXINS,DNA-DAMAGE,HEP G2,B-1,ROS,CYTOTOXICITY,MITOCHONDRIA,EXPRESSION,APOPTOSIS,DEOXYNIVALENOL,fumonisin B1,aflatoxin B1,cytotoxicity,mitochondrial toxicity}}, language = {{eng}}, number = {{13}}, pages = {{20}}, title = {{Bioenergetic status of the intestinal and hepatic cells after short term exposure to fumonisin B1 and aflatoxin B1}}, url = {{http://doi.org/10.3390/ijms23136945}}, volume = {{23}}, year = {{2022}}, }
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