UCLA

Per- and polyfluoroalkyl substances (PFAS) are among the most prevalent and persistent environmental toxicants worldwide. The scale of human exposure to PFAS is vast and available data indicate that PFAS can target most organ systems in the body and produce a wide range of health effects. The molecular mechanisms eliciting these effects are incompletely understood and further characterization is needed to better protect public health. Considering that many PFAS are surface active substances, they have the potential to alter phase separation dynamics within a cell and may particularly target biomolecular condensates (BCs), subcellular compartments that are dependent upon their physical organization to execute their regulatory functions. In this work, the reproductive system of Caenorhabditis elegans was used as a model to examine the ability of two surfactant PFAS, PFOS and F-53B, to disrupt BC structure and function. Both PFOS and F-53B were found to alter the structure of P granules and the synaptonemal complex (SC), two BCs essential for proper germ cell development in C. elegans. In sensitized P granule and SC mutants, PFOS and F-53B exposures exacerbated infertility and embryonic lethality defects. These results indicate that the impacts of PFAS exposure on BC structure have functional consequences and that BCs may play a role in mediating PFAS-induced reproductive toxicity. Furthermore, this work suggests it is plausible that BC structural disruption could serve as a molecular initiating event for PFAS-induced toxicity in other cell types and organisms.