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Multiomics Analysis of PCB126's Effect on a Mouse Chronic-Binge Alcohol Feeding Model
Tyler C Gripshover1,2,3, Banrida Wahlang1,2,3,4, Kimberly Z Head2,5
1Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, Kentucky, USA.
Environmental Health Perspectives
|April 15, 2024
Summary
Polychlorinated biphenyl (PCB) 126 exposure exacerbates alcohol-associated liver disease (ALD) by altering gene expression and reducing essential metal levels in mice. This suggests pollutants contribute to malnutrition in ALD.
Area of Science:
- Environmental Health
- Toxicology
- Hepatology
Background:
- Environmental pollutants like polychlorinated biphenyls (PCBs) are linked to liver disease pathogenesis.
- Previous research showed PCB126 promotes steatosis and modulates metabolism in alcohol-associated liver disease (ALD).
Purpose of the Study:
- To investigate the mechanistic hypotheses behind PCB126's promotion of ALD.
- To elucidate how PCB126 modifies the liver's molecular landscape in the context of alcohol consumption.
Main Methods:
- Mice were exposed to PCB126 and ethanol (EtOH) using a chronic-binge model.
- Liver tissues underwent mRNA sequencing, phosphoproteomics, and metal quantification via ICP-MS.
Main Results:
- PCB126 uniquely altered the transcriptome in EtOH-fed mice, increasing differentially expressed genes.
- Gene ontology analysis revealed impacts on peptidyl tyrosine modifications and metal/ion/zinc binding.
- PCB126 exposure significantly reduced hepatic magnesium, cobalt, and zinc levels in EtOH-fed mice.
Conclusions:
- PCB126 modifies ALD, potentially by contributing to malnutrition through metal deficiency.
- Environmental pollutants like PCBs may worsen ALD prognosis by impacting essential nutrient levels.
