Metabolomics and lipidomics to identify biomarkers of effect related to exposure to non-dioxin-like polychlorinated biphenyls in pigs

Hernández‐Mesa, Maykel; Narduzzi, Luca; Ouzia, Sadia; Soetart, Nicolas; Jaillardon, Laëtitia; Guitton, Yann; Bizec, Bruno Le

doi:10.1016/j.chemosphere.2022.133957

Cited by 10 publications

(2 citation statements)

References 73 publications

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“…It is also noteworthy that the most recent studies in toxicology are focused on exposure to low-dose pollutant mixtures to better simulate the environmental conditions in real life. The early results suggest that low dose mixtures could induce dysmetabolism and pollutants could have a synergistic effect on systemic inflammatory response, highlighting the need for policy makers to reassess the threshold values in risk assessment and improve the strategies to protect human health [206][207][208] intervention strategy to alleviate the burden of immune system pathologies involves targeted environmental management and public health initiatives. In 2018, Bourguignon and coworkers proposed an approach aimed at reducing the exposure to complex mixtures during pregnancy by implementing global initiatives to mitigate the possible consequences of combinations of adverse lifestyle factors.…”

Section: Discussionmentioning

confidence: 99%

Guardians Under Siege: Exploring Pollution's effects on Human Immunity

Drago,

Aloi,

Ruggieri

et al. 2024

Preprint

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Chemical pollution poses a significant threat to human health, with detrimental effects on various physiological systems, including the respiratory, cardiovascular, mental, and perinatal domains. While the impact of pollution on these systems has been extensively studied, the intricate relationship between chemical pollution and immunity remains a critical area of investigation. The focus of this study is to elucidate the relationship between chemical pollution and human immunity. To accomplish this task, this study presents a comprehensive review that encompasses in vitro, ex vivo, and in vivo studies, shedding light on the ways in which chemical pollution can modulate human immunity. Our aim is to unveil the complex mechanisms by which environmental contaminants compromise the delicate balance of the body's defence systems going beyond the well-established associations with defence system delving into the less-explored link between chemical exposure and various immune disorders, adding urgency to our understanding of the underlying mechanisms and their implications for public health.

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Section: Discussionmentioning

confidence: 99%

Guardians Under Siege: Exploring Pollution's effects on Human Immunity

Drago,

Aloi,

Ruggieri

et al. 2024

Preprint

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“…Additionally, AFB1 induces oxidative stress and lipid peroxidation, as well as affecting the peroxisome proliferator-activated receptor Gamma (PPARγ) pathway, which is involved in lipid signaling [ 15 , 16 , 17 ]. Lipidomics can characterize the profile of lipid molecules within organisms and can be used to identify biomarkers of contaminant toxicity [ 18 , 19 ]. However, there is limited research on the disruption of intracellular lipid molecular metabolism caused by AFB1.…”

Section: Introductionmentioning

confidence: 99%

AFB1 Triggers Lipid Metabolism Disorders through the PI3K/Akt Pathway and Mediates Apoptosis Leading to Hepatotoxicity

Wang,

Li,

Liao

et al. 2024

Foods

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As the most prevalent mycotoxin in agricultural products, aflatoxin B1 not only causes significant economic losses but also poses a substantial threat to human and animal health. AFB1 has been shown to increase the risk of hepatocellular carcinoma (HCC) but the underlying mechanism is not thoroughly researched. Here, we explored the toxicity mechanism of AFB1 on human hepatocytes following low-dose exposure based on transcriptomics and lipidomics. Apoptosis-related pathways were significantly upregulated after AFB1 exposure in all three hES-Hep, HepaRG, and HepG2 hepatogenic cell lines. By conducting a comparative analysis with the TCGA-LIHC database, four biomarkers (MTCH1, PPM1D, TP53I3, and UBC) shared by AFB1 and HCC were identified (hazard ratio > 1), which can be used to monitor the degree of AFB1-induced hepatotoxicity. Simultaneously, AFB1 induced abnormal metabolism of glycerolipids, sphingolipids, and glycerophospholipids in HepG2 cells (FDR < 0.05, impact > 0.1). Furthermore, combined analysis revealed strong regulatory effects between PIK3R1 and sphingolipids (correlation coefficient > 0.9), suggesting potential mediation by the phosphatidylinositol 3 kinase (PI3K) /protein kinase B (AKT) signaling pathway within mitochondria. This study revealed the dysregulation of lipid metabolism induced by AFB1 and found novel target genes associated with AFB-induced HCC development, providing reliable evidence for elucidating the hepatotoxicity of AFB as well as assessing food safety risks.

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