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Environmental dose of Bisphenol S exposure to brown adipose tissue accelerates aging

ABSTRACT: Bisphenol S (BPS), a common industrial chemical, is increasingly recognized for its potential to disrupt physiological functions even at environmental doses. In this study, we investigated the effects of BPS exposure on lifespan and health span using Caenorhabditis elegans and mouse models. We found that BPS accumulates in brown adipose tissue (BAT), inducing BAT aging by triggering mitochondrial dysfunction, chronic inflammation, altered intercellular communication, cellular senescence, deregulated nutrient-sensing pathways, impaired macroautophagy, and loss of proteostasis. These changes accelerated aging in multiple organs, including the heart, liver, kidneys, lungs, and skeletal muscle. Notably, BAT transplantation experiments revealed that BAT from BPS-exposed mice induced accelerated aging in non-exposed mice, while BAT from non-exposed mice mitigated aging in BPS-exposed mice. In summary, this study is the first to demonstrate that environmental doses of BPS promote systemic aging by disrupting BAT energy metabolism.

ORGANISM(S): Mus musculus

PROVIDER: GSE277525 | GEO | 2024/09/20

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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Environmental dose of Bisphenol S exposure to brown adipose tissue accelerates aging

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