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Bacteria covalently incorporate polyfluoroalkyl carboxylates into membrane lipids

ABSTRACT: Per- and polyfluoroalkyl substances (PFASs) are global contaminants of concern to human and environmental health 1. Little is known about biological attenuation processes and microbiota PFAS interactions. Here we show that the soil bacterium Pseudomonas sp. strain 273 covalently incorporates polyfluoroalkyl carboxylates (FTCAs) including 8:3 FTCA into phosphatidylethanolamine (PE) and phosphatidylglycerol (PG), two prominent components of lipid bilayers. Semi-quantitative lipidomic analysis estimated that 7.5% of the bacteriums phospholipid pool contained 8:3 FTCA, resulting in a PFAS membrane incorporation factor (MIF) of 423. Synthesis of PE and PG species carrying a polyfluorocarbon acyl tail was observed in five other axenic bacterial cultures tested, albeit with lower MIFs. Our results suggest that the formation of fluoromembranes is a prevalent bacterial process potentially impacting the fate, longevity, bioaccumulation, and biomagnification of certain PFASs.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Pseudomonas Sp. 273 (ncbitaxon:75692)

SUBMITTER: Paul Abraham

PROVIDER: MSV000098309 | MassIVE | Tue Jun 24 17:43:00 BST 2025

SECONDARY ACCESSION(S): PXD065413

REPOSITORIES: MassIVE

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Project description:Per- and polyfluoroalkyl substances (PFAS) are some of the most prominent organic contaminants in human blood that have the potential to disrupt biological processes and pathways in the liver. Although the toxicological implications from human exposure to perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are well established, data on other, lesser-understood PFAS are limited. A challenge for regulatory authorities is to determine acceptable levels of human exposure to large, diverse classes of environmental contaminants. New approach methodologies (NAMs) that apply bioinformatics tools to interpret biological data are being increasingly considered to inform risk assessment when traditional toxicology methodologies are not amenable. The aim of the current investigation was to identify the biological responses relevant to PFAS mode of action as the concentration (benchmark dose) that these effects take place in order to utililze this information to inform/facilitate read-across for risk assessment of data-poor PFAS. A TempO-Seq platform (BioSpyder) measured gene expression changes in human liver microtissues (i.e., spheroids) after 1-day and 10-day exposures to increasing concentrations of PFAS. A bioinformatics framework was applied to 23 PFAS sub-classed into carboxylates (PFCAs), sulfonates (PFSAs), or PFAS precursors that were analyzed for the total altered transcripts, the concentration where effects take place, and identifying target genes of interest. Both PFCAs and PFSAs exhibited a trend toward increased transcriptional changes with carbon chain-length. Specifically, longer-chain compounds (7 to 10 carbons) were more likely to surpass liver-toxic transcriptomic thresholds established from previous studies than shorter chain PFAS. Longer-chain PFAS were also more potent, inducing transcriptional effects at lower concentrations. However, PFOS was the most potent PFAS and of all precursors, only PFOSA (a PFOS precursor) induced a response. The combined high-throughput transcriptomic and bioinformatics analyses revealed the capability of NAMs to assess the effects of PFAS in liver microtissues; such data improves our understanding of PFAS-related effects in humans and facilitates the use of read-across in human health risk assessment for other data-poor chemicals.

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Bacteria covalently incorporate polyfluoroalkyl carboxylates into membrane lipids

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