Perfluorooctane sulfonic acid impairs spermatogenesis via the liver-gut microbiota-testis axis: a central role of chenodeoxycholic acid metabolism.
Level 5 - mechanism / opinion, no new human data
Bench and animal research with no human data
PubMed 40554061 · doi:10.1016/j.jare.2025.06.037
What was done
The authors investigated the mechanisms of perfluorooctane sulfonic acid (PFOS) reproductive toxicity in a murine model. Testicular single-nucleus transcriptome sequencing, serum metabolomic profiling, and hepatic transcriptome datasets were analyzed. Mechanistic experiments evaluated the liver-gut microbiota-testis axis using chenodeoxycholic acid (CDCA) intervention, fecal microbiota transplantation, metagenomic sequencing, testicular and Ligilactobacillus murinus metabolomics, and direct L. murinus administration.
What was found
The abstract reports no numerical data, effect sizes, or statistical values. Qualitatively, PFOS exposure caused spermatogenic arrest and an altered testicular microenvironment in mice. Hepatic CDCA synthesis was repressed by PFOS, which reduced serum and testicular levels of linoleic acid, retinol, and vitamin D3. Furthermore, reduced CDCA lowered the gut abundance of L. murinus, which impaired spermatogenesis through pathways potentially involving aspartic acid metabolism.
Why it matters
This study outlines a multi-organ mechanism linking PFOS exposure to impaired spermatogenesis through altered hepatic bile acid synthesis and gut microbiota disruption.
Limits
The study was conducted entirely in a rodent model, so direct applicability to human male fertility is unproven. The abstract omits sample sizes, exposure doses, treatment durations, and all quantitative metrics.
Cited by
- supports PFAS chemicals are linked to health issues including hormone disruption, gut microbiome disruption, and fertility issues.