Imptox research published in the International Journal of Molecular Science
A group of Imptox scientists from Ghent University published their findings on the effects of mycotoxins on the bioenergetic status of intestinal and liver cells.
Mycotoxins are among the most common toxic contaminants of a series of foods and feed all around the world. In this study, Imptox scientists evaluated in particular two types of mycotoxins, FB1 and AFB1, to understand their effect on mitochondria in intestinal and hepatic cells after short-term exposure to these contaminants.
Their study shows for the first time that toxins have an impact on cell bioenergetics and the ability of cells to cope with extra stress and energy demands and that the impact varies depending on the specific toxin and cell type. This research will form a basis for further future studies of co-exposure and effects of mycotoxins with other contaminants, such as the omnipresent microplastics.
Imptox scientists and contributing authors: Mohamed F. Abdallah, Charlotte Grootaert, and Andreja Rajkovic
Further authors: Xiangrong Chen
International Journal of Molecular Science, June 2022
Bioenergetic Status of the Intestinal and Hepatic Cells after Short Term Exposure to Fumonisin B1 and Aflatoxin B1
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.