Yangtze finless porpoise (YFP) is a critically endangered species in China. It has been found that YFP is constantly exposed to perfluorooctane sulfonate (PFOS) in aquatic environments, leading to significant bioaccumulation. However, the impacts of PFOS on YFP health and survival are still unknown. To circumvent the limitations in YFP research, this study used YFP umbilical cord fibroblast cell line and exposed the cells to PFOS for 48 h, with objectives to uncover the cytotoxicity and mechanisms of PFOS in YFP. A high-throughput proteomics assay showed that PFOS exposure at 50 μM for 48 h perturbed the proteome structure in YFP umbilical cord fibroblast cells. Functional annotation found the high relevance of oxidative stress, mitochondrial oxidative phosphorylation, and DNA damage to PFOS cytotoxic mechanisms. Concordantly, PFOS exposure significantly increased the deposition of reactive oxygen species (ROS) in YFP cells. The potential of mitochondria to produce ATP was also compromised by PFOS, which was accompanied by the higher permeability of mitochondrial membrane. In addition, exposure of YFP umbilical cord fibroblast cells to 50 μM PFOS damaged the DNA assembly as evidenced by the increase in the percentage of DNA fragmentation. Gene transcription and enzymatic activity of caspases were up-regulated by PFOS, subsequently favoring the occurrence of early and late apoptosis. It was notable that ROS scavenger could successfully mitigate the cytotoxicity of PFOS on oxidative stress and apoptosis, thus pinpointing ROS as the molecular initiating event in apoptosis endpoints. To our knowledge, this is the first study that investigates the detrimental effects of PFOS using YFP umbilical cord fibroblast cells. The data will support an accurate assessment of ecological risks imposed by environmental pollutants on the health and sustainability of YFP, which is especially important under the context of sharp decline in YFP population and national initiative in YFP conservation.

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http://dx.doi.org/10.1016/j.scitotenv.2024.178030DOI Listing

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