Mitochondrial Damage Induced by T-2 Mycotoxin on Human Skin-Fibroblast Hs68 Cell Line.
Edyta JanikMichal CeremugaMarcin NiemcewiczEwelina SynowiecTomasz SliwińskiMichał BijakPublished in: Molecules (Basel, Switzerland) (2023)
T-2 toxin is produced by different Fusarium species and belongs to the group of type A trichothecene mycotoxins. T-2 toxin contaminates various grains, such as wheat, barley, maize, or rice, thus posing a risk to human and animal health. The toxin has toxicological effects on human and animal digestive, immune, nervous and reproductive systems. In addition, the most significant toxic effect can be observed on the skin. This in vitro study focused on T-2 toxicity on human skin fibroblast Hs68 cell line mitochondria. In the first step of this study, T-2 toxin's effect on the cell mitochondrial membrane potential (MMP) was determined. The cells were exposed to T-2 toxin, which resulted in dose- and time-dependent changes and a decrease in MMP. The obtained results revealed that the changes of intracellular reactive oxygen species (ROS) in the Hs68 cells were not affected by T-2 toxin. A further mitochondrial genome analysis showed that T-2 toxin in a dose- and time-dependent manner decreased the number of mitochondrial DNA (mtDNA) copies in cells. In addition, T-2 toxin genotoxicity causing mtDNA damage was evaluated. It was found that incubation of Hs68 cells in the presence of T-2 toxin, in a dose- and time-dependent manner, increased the level of mtDNA damage in both tested mtDNA regions: NADH dehydrogenase subunit 1 (ND1) and NADH dehydrogenase subunit 5 (ND5). In conclusion, the results of the in vitro study revealed that T-2 toxin shows adverse effects on Hs68 cell mitochondria. T-2 toxin induces mitochondrial dysfunction and mtDNA damage, which may cause the disruption of adenosine triphosphate (ATP) synthesis and, in consequence, cell death.
Keyphrases
- escherichia coli
- mitochondrial dna
- cell death
- induced apoptosis
- oxidative stress
- cell cycle arrest
- copy number
- reactive oxygen species
- healthcare
- endothelial cells
- public health
- endoplasmic reticulum stress
- stem cells
- dna damage
- mental health
- cell proliferation
- emergency department
- signaling pathway
- dna methylation
- cell therapy
- genome wide
- gene expression
- social media
- adverse drug
- oxide nanoparticles