T-2 toxin, as a highly toxic mycotoxin to humans and animals, induces oxidative stress and apoptosis in various cells and tissues. Apoptosis and mitochondrial fusion/fission are two tightly interconnected processes that are crucial for maintaining physiological homeostasis. However, the role of mitochondrial fusion/fission in apoptosis of T-2 toxin remains unknown. Hence, we aimed to explore the putative role of mitochondrial fusion/fission on T-2 toxin induced apoptosis in normal human liver (HL-7702) cells. T-2 toxin treatment (0, 0.1, 1.0, or 10 μg/L) for 24 h caused decreased cell viability and ATP concentration and increased production of (ROS), as seen by a loss of mitochondrial membrane potential (∆Ψm) and increase in mitochondrial fragmentation. Subsequently, the mitochondrial dynamic imbalance was activated, evidenced by a dose-dependent decrease and increase in the protein expression of mitochondrial fusion (OPA1, Mfn1, and Mfn2) and fission (Drp1 and Fis1), respectively. Furthermore, the T-2 toxin promoted the release of cytochrome c from mitochondria to cytoplasm and induced cell apoptosis triggered by upregulation of Bax and Bax/Bcl-2 ratios, and further activated the caspase pathways. Taken together, these results indicate that altered mitochondrial dynamics induced by oxidative stress with T-2 toxin exposure likely contribute to mitochondrial injury and HL-7702 cell apoptosis.
A reliable and sensitive analytical method was developed for simultaneous determination of deoxynivalenol(DON), 3-acetyldeoxynivalenol (3-ADON), 15-acetyldeoxynivalenol (15-ADON), fusarenon X (FUS-X), and masked deoxynivalenol (deoxynivalenol-3-glucoside, D3G) in formula feed, concentrated feed, and premixed feed products. The method was based on an improved sample pretreatment with the commercially available HLB cartridges used for sample purification and enrichment followed by analysis using ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS). Several key parameters including the extraction solvents, the positions of sample loading solvents, washing and elution solvents for HLB cartridges were carefully optimized to achieve optimal extraction and purification efficiencies. The established method was extensively validated by determining the linearity (R2 ≥ 0.99), sensitivity (limit of quantification in the range of 0.08–4.85 μg/kg), recovery (79.3%–108.1%), precision (Intra-day RSDs ≤ 13.5% and Inter-day RSDs ≤ 14.9%), and then was successfully applied to determine the four type B trichothecenes and D3G in a total of 31 feed samples. Among them, 26 were contaminated with various mycotoxins at the levels of 2.1–864.5 μg/kg, and D3G has also been detected in 17 samples with the concentrations in the range of 2.1–34.8 μg/kg, proving the established method to be a valuable tool for type B trichothecenes and masked DON monitoring in complex feed matrices.
This biomonitoring study was conducted to investigate the concentration levels of five Alternaria mycotoxins in urine samples from 269 healthy volunteers living in the Yangtze River Delta, China. Alternariol (AOH), alternariol monomethyl ether (AME), tenuazonic acid (TeA) and tentoxin (TEN) were detected in 38.3%, 48.7%, 63.9% and 23.4% of urine samples with the concentrations ranging from 0.057 to 45.8 ng/mL, 0.020 to 0.802 ng/mL, 0.050 to 80.6 ng/mL and 0.021 to 0.939 ng/mL, respectively. Altenuene (ALT) was not detected in any urine sample. Based on the urinary concentrations, the probable daily intake (PDI) values of Alternaria mycotoxins were calculated, and 100%, 99.2–100%, 0.372% and 1.12% of participants exceeded the threshold of toxicological concern (TTC) values for AOH, AME, TeA and TEN, respectively. This study revealed high potential health risks related to the contaminations of major Alternaria mycotoxins in China and highlighted the necessity for more toxicological studies to provide better basis for further comprehensive risk assessments.