<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Mohamed F Abdallah</style></author><author><style face="normal" font="default" size="100%">Jessa May Recote</style></author><author><style face="normal" font="default" size="100%">Camille Van Camp</style></author><author><style face="normal" font="default" size="100%">Wannes Van Hassel</style></author><author><style face="normal" font="default" size="100%">Pedroni, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Luca Dellafiora</style></author><author><style face="normal" font="default" size="100%">Julien Masquelier</style></author><author><style face="normal" font="default" size="100%">Rajkovic, Andreja</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Potential (co-)contamination of dairy milk with AFM1 and MC-LR and their synergistic interaction in inducing mitochondrial dysfunction in HepG2 cells.</style></title><secondary-title><style face="normal" font="default" size="100%">Food Chem Toxicol</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Aflatoxin M1</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">Food Contamination</style></keyword><keyword><style  face="normal" font="default" size="100%">Hep G2 Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Marine toxins</style></keyword><keyword><style  face="normal" font="default" size="100%">Membrane Potential, Mitochondrial</style></keyword><keyword><style  face="normal" font="default" size="100%">microcystins</style></keyword><keyword><style  face="normal" font="default" size="100%">milk</style></keyword><keyword><style  face="normal" font="default" size="100%">Mitochondria</style></keyword><keyword><style  face="normal" font="default" size="100%">Tandem Mass Spectrometry</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2024</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2024 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">192</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Several toxic metabolites, such as aflatoxin M1 (AFM1), are known to contaminate dairy milk. However, as mentioned in an external EFSA report, there is a knowledge gap regarding the carry-over of certain emerging toxins such as microcystin-LR (MC-LR). Therefore, this work aimed to develop an LC-MS/MS method for MC-LR quantification in dairy milk. Also, the method included AFM1 as a common fungal metabolite and applied to analyze 113 dairy milk samples collected directly after the end of the summer peak. Both toxins were below their LODs, keeping the question on MC-LR carry-over still unanswered. Moreover, an in silico analysis, using a 3D molecular modeling was performed, pointing to a possible interaction between MC-LR and milk proteins, especially β-lactoglobulin. Since AFM1 and MC-LR are hepatotoxic, their interaction in inducing mitochondrial dysfunction in HepG2 cells was investigated at low (subcytotoxic) concentrations. Live cell imaging-based assays showed an inhibition in cell viability, without involvement of caspase-3/7, and a hyperpolarization in the mitochondrial membrane potential after the exposure to a mixture of 100&amp;nbsp;ng&amp;nbsp;mL AFM1 and 1000&amp;nbsp;ng&amp;nbsp;mL MC-LR for 48h. Extracellular flux analysis revealed inhibitions of several key parameters of mitochondrial function (basal respiration, ATP-linked respiration, and spare respiratory capacity).&lt;/p&gt;
</style></abstract></record></records></xml>