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Guo X.,CAS Hefei Institutes of Physical Science | Guo X.,Anhui Academy of Agricultural Sciences | Li Q.,CAS Hefei Institutes of Physical Science | Shi J.,CAS Hefei Institutes of Physical Science | And 8 more authors.
Chemosphere | Year: 2016

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. © 2016 Elsevier Ltd. Source

Zhao Y.,CAS Hefei Institutes of Physical Science | Ma X.,CAS Institute of Biophysics | Wang J.,CAS Hefei Institutes of Physical Science | Wang J.,Key Laboratory of Environmental Toxicology and Pollution Control Technology of Anhui Province | And 10 more authors.
Radiation Research | Year: 2015

Previously reported studies have demonstrated the involvement of p21Waf1/CIP1 in radiation-induced bystander effects (RIBE). Mouse embryonic fibroblasts (MEFs) lacking Hus1 fail to proliferate in vitro, but inactivation of p21 allows for the continued growth of Hus1-deficient cells, indicating the close connection between p21 and Hus1 cells. In this study, wild-type MEFs, Hus1+/+p21-/- MEFs and p21-/-Hus1-/- MEFs were used in a series of radiation-induced bystander effect experiments, the roles of p21 and Hus1 in the induction and transmission of radiation-induced damage signals were investigated. Our results showed that after 5 cGy α particle irradiation, wild-type MEFs induced significant increases in γ-H2AX foci and micronuclei formation in bystander cells, whereas the bystander effects were not detectable in p21-/-Hus1+/+ MEFs and were restored again in p21-/-Hus1-/- MEFs. Media transfer experiments showed that p21-/-Hus1+/+ MEFs were deficient in the production bystander signals, but could respond to bystander signals. We further investigated the mitogen-activated protein kinases (MAPKs) that might be involved in the bystander effects. It was found that although knocking out p21 did not affect the expression of connexin43 and its phosphorylation, it did result in inactivation of some MAPK signal pathway kinases, including JNK1/2, ERK1/2 and p38, as well as a decrease in reactive oxygen species (ROS) levels in irradiated cells. However, the activation of MAPK kinases and the ROS levels in irradiated cells were restored in the cell line by knocking out Hus1. These results suggest that p21Waf1/CIP1 and Hus1 play crucial roles in the generation and transmission of bystander damage signals after low-dose α-particle irradiation. © 2015 by Radiation Research Society. Source

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