Bioenergetic Status of the Intestinal and Hepatic Cells after Short Term Exposure to Fumonisin B1 and Aflatoxin B1.
aflatoxin B1
cytotoxicity
fumonisin B1
mitochondrial toxicity
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
22 Jun 2022
22 Jun 2022
Historique:
received:
23
03
2022
revised:
20
06
2022
accepted:
21
06
2022
entrez:
9
7
2022
pubmed:
10
7
2022
medline:
14
7
2022
Statut:
epublish
Résumé
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
Identifiants
pubmed: 35805950
pii: ijms23136945
doi: 10.3390/ijms23136945
pmc: PMC9267062
pii:
doi:
Substances chimiques
Fumonisins
0
Reactive Oxygen Species
0
fumonisin B1
3ZZM97XZ32
Aflatoxin B1
9N2N2Y55MH
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
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