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Transcriptomic profiling of mouse colorectal organoids following NAP treatment.

ABSTRACT: Bisphenol F (BPF) is a widely used substitute for bisphenol A (BPA) in plastic manufacturing; however, its potential toxicity remains insufficiently characterized. In this study, we investigated the impact of BPF exposure on the intestinal barrier and cardiovascular system. Based on prior untargeted metabolomic analysis, we revealed that BPF can be converted into N-acetylputrescine (NAP) through a microbiota-associated metabolic process. Further experiments demonstrated that BPF exposure stimulated intestinal epithelial cells to secrete spermidine/spermine N1-acetyltransferase 1 (Sat1), an enzyme involved in this conversion. To explore the molecular mechanisms underlying NAP-induced effects, we performed RNA sequencing on mouse colorectal organoids treated with NAP. Transcriptomic analysis was conducted to identify gene expression changes and signaling pathways associated with NAP exposure. The raw sequencing data and processed expression matrices are provided in this submission.

ORGANISM(S): Mus musculus

PROVIDER: GSE324667 | GEO | 2026/03/15

REPOSITORIES: GEO

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Project description:Bisphenols are used in the process of polymerization of polycarbonate plastics and epoxy resins, which have numerous applications in a variety of consumer products. Due to their hydrophobic properties, bisphenols can easily migrate out of plastic products especially into fatty foods. They have been found in brain, liver, adipose tissue and body fluids, illustrating their environmental prevalence. By increasing colonic inflammation in mice, disrupting the intestinal bacterial community structure and altering the microbial membrane transport system in zebrafish, bisphenols seem to interfere with the gut microbiome. The highly abundant human commensal bacterium Bacteroides thetaiotaomicron was exposed to bisphenols (Bisphenol A (BPA), Bisphenol F (BPF), Bisphenol S (BPS)), to examine the mode of action, in particular of BPF. All chemicals caused a concentration-dependent growth inhibition and the half-maximal effective concentration (EC50) corresponded to their individual logP values, a measure of their hydrophobicity. B. thetaiotaomicron exposed to BPF decreased membrane fluidity with increasing BPF concentrations. Physiological changes including an increase of acetate concentration were observed in cells treated with 0.57 mM BPF. On the proteome level, a higher abundance of several ATP synthase subunits and multidrug efflux pumps suggested an increased energy demand for adaptive mechanisms after BPF exposure. Defence mechanisms were also implicated by a pathway analysis, that identified a higher abundance of members of resistance pathways/strategies to cope with xenobiotics (i.e. antibiotics). Here, we present further insights into the mode of action of bisphenols in a human commensal gut bacterium regarding growth inhibition, and the physiological and functional state of the cell. These results, combined with microbiota-directed effects, could lead to a better understanding of host health disturbances and disease development based on xenobiotic uptake.

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Transcriptomic profiling of mouse colorectal organoids following NAP treatment.

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