Preconception exposure to perfluorooctanesulfonic acid (PFOS) and perfluorobutanesulfonic acid (PFBS) impaired reproduction via insulin/insulin-like growth factor signaling pathway without effects on the second generation in Caenorhabditis elegans.

In previous studies, preconception exposure to perfluorooctanesulfonic acid (PFOS) and perfluorobutanesulfonic acid (PFBS) reduced the reproductive capacity and altered the development of the offspring of C. elegans. However, the specific pathways involved in these observations were not determined. Thus, we investigated how preconception exposure to PFOS (40 μM) and PFBS (2000 μM) affected embryonic nutrient loading and offspring development. Preconception exposure to 40 μM PFOS significantly reduced nutrient loading to embryos via vit-6 (vitellogenin) and rme-2 (low-density lipoprotein particle receptor). The insulin/insulin-like growth factor signaling pathway (IIS), daf-2 (homolog of human insulin receptor precursor) and daf-16 (homolog of human forkhead box O) played a role in altering the reproductive capacity caused by preconception exposure to PFOS. Preconception exposure to PFBS did not affect nutrient loading but reduced reproductive health via IIS as well as nhr-49 (homolog of human hepatocyte nuclear factor 4α). In addition, preconception exposure to PFOS or PFBS resulted in no multigenerational effects on the reproductive health of F1 offspring worms. Preconception exposure to PFOS disrupted parental nutrient production and loading, reproduction, and offspring development, while PFBS impaired lipid metabolism and offspring development at higher doses than PFOS.