Xenobiotic-induced liver injury: Molecular mechanisms and disease progression.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic and observational studies without systematic synthesis
PubMed 40845633 · doi:10.1016/j.ecoenv.2025.118854
What was done
This narrative review synthesized evidence from experimental in vivo models and human cohort studies examining how diverse classes of environmental xenobiotics (including aflatoxins, alcohol, PCBs, PFAS, PAHs, pesticides, heavy metals, BPA, aristolochic acids, cyanotoxins, and nitrosamines) cause liver injury across varying exposure paradigms.
What was found
The abstract reports no quantitative values or statistical effect sizes. Qualitatively, it reports that chronic low-dose exposures promote progressive hepatic pathologies—including steatosis, fibrosis, cholestasis, drug-induced liver injury, and hepatocellular carcinoma. Reported pathways include cytochrome P450-mediated bioactivation, oxidative stress, mitochondrial dysfunction, DNA damage, immune dysregulation, altered gut microbiota composition, and disruption of nuclear receptors including PPARα, CAR, and AhR, with disease progression modified by host factors and viral co-infections.
Why it matters
It consolidates disparate molecular pathways through which common environmental toxicants alter liver metabolism and immunity, emphasizing the combined impact of low-dose chronic exposures and biological co-factors.
Limits
The abstract describes a broad narrative synthesis rather than a systematic review with defined search strings or quality grading. No numerical outcomes, exposure thresholds, or human effect sizes are provided, and findings rely heavily on preclinical mechanistic models.
Cited by
- supports The liver does not store toxins; its function is detoxification and converting poisons into harmless particles.