Aflatoxin promotes signs of liver cell aging in mice
Mouse experiments implicated a chemical-sensing protein in the toxin’s effects, highlighting a potential target for toxin-related liver disease.
Limit: The abstract does not report doses, exposure durations, or results by experimental system
Edited by Boris Djordjevic · AgingResearch.News
Experiments in mice and AML-12 cells grown in the lab examined how aflatoxin B1, an environmental liver toxin, promoted senescence, a state in which cells stop dividing. The researchers focused on the aryl hydrocarbon receptor, a protein that responds to chemical signals.
Across these experiments, they reported that toxin exposure increased the receptor’s levels and promoted its movement into the cell nucleus, which contains DNA. Exposure also caused breaks in both strands of DNA, activated proteins that halt cell division and increased inflammatory signals associated with senescence. Inhibiting the receptor with a chemical called CH223191 reversed the reported liver cell injury and senescence markers. The authors identified the receptor as a potential target for aflatoxin-related liver disease.
Why it matters
Understanding how environmental toxins promote liver cell senescence may help identify ways to address toxin-related liver disease.
Caveats
These experiments involved mice and lab-grown cells, not people. The abstract does not separate the results by experimental system or report doses and exposure durations.
The paper
Yunnan Agricultural University
Journal of Agricultural and Food Chemistry, Oct 25, 2026
