Perfluorooctane sulfonate exposure causes gonadal developmental toxicity in Caenorhabditis elegans through ROS-induced DNA damage.

Abstract

Perfluorooctane sulfonate (PFOS), a common persistent organic pollutant, has been reported to show potential developmental toxicity in many animal studies. However, little was known about its effects on reproductive tissues, especially in the germ line. In the present study, Caenorhabditis elegans was used as an in vivo experimental model to study the developmental toxicity caused by PFOS exposure, especially in the gonads. Our results showed that PFOS exposure significantly retarded gonadal development, as shown by the increased number of worms that remained in the larval stages after hatched L1-stage larvae were exposed to PFOS for 72 h. Investigation of germ line proliferation following PFOS exposure showed that the number of total germ cells reduced in a dose-dependent manner when L1-stage larvae were exposed to 0-25.0 μM PFOS. PFOS exposure induced transient mitotic cell cycle arrest and apoptosis in the germ line. Quantification of DNA damage in proliferating germ cells and production of reactive oxygen species (ROS) showed that distinct foci of HUS-1:GFP and ROS significantly increased in the PFOS-treated groups, whereas the decrease in mitotic germ cell number and the enhanced apoptosis induced by PFOS exposure were effectively rescued upon addition of dimethyl sulfoxide (DMSO) and mannitol (MNT). These results suggested that ROS-induced DNA damage might play a pivotal role in the impairment of gonadal development indicated by the reduction in total germ cells, transient mitotic cell cycle arrest, and apoptosis.