With the regulation of perfluorooctanesulfonate (PFOS), 6:2 chlorinated polyfluoroalkyl ether sulfonate (6:2 Cl-PFESA) has been used as a potential PFOS alternative in electroplating . In this study, the uptake, translocation and phytotoxicity of PFOS and 6:2 Cl-PFESA in mung bean ( Vigna radiata (Linn.) Wilczek. ) were investigated. The uptake kinetics of PFOS and 6:2 Cl-PFESA fit the Michaelis-Menten equation well, suggesting that the uptake is a carrier-mediated process. The root concentration factor (RCF) of 6:2 Cl-PFESA (34.55 mL g −1 dw) was 1.27 times that of PFOS (27.11 mL g −1 dw), and the translocation factor (TF) of 6:2 Cl-PFESA (0.177) was 1.07 times that of PFOS (0.165). Exposure to 6:2 Cl-PFESA and PFOS both resulted in the inhibition of mung bean seedling development. Treatment with 6:2 Cl-PFESA and PFOS led to the concentration-dependent elevation of malondialdehyde (MDA), carbonyl groups, and phosphorylated histone H2AX (γ-H2AX) levels in mung bean roots. The MDA and carbonyl group contents induced by 6:2 Cl-PFESA were 1.10–1.35 and 1.03–1.14 times, respectively, those of PFOS. The hydroxyl free radical (·OH) levels in mung bean roots after exposure to PFOS and 6:2 Cl-PFESA were elevated significantly, and the ·OH levels induced by 6:2 Cl-PFESA were higher than those induced by PFOS. Hydroxyl free radical levels were positively correlated with the MDA and carbonyl group contents in mung bean roots ( p < 0.05). The dynamic changes in some antioxidative enzyme activities in mung bean seedlings were determined, including peroxidase (POD), superoxide dismutase (SOD), and catalase (CAT). The results demonstrated the phytotoxicities of 6:2 Cl-PFESA and PFOS to mung bean in the early developmental stage. 6:2 Cl-PFESA is more harmful to mung beans than PFOS. The production of hydroxyl radical is the mechanism that causes the toxicity of PFOS and 6:2 Cl-PFESA toward plants.
Hui Dong,Demei Xu,Lihua Hu,Lingrui Li,Erqun Song,Yang Song
Tetrachlorobenzoquinone (TCBQ) is an active metabolite of pentachlorophenol (PCP). Although the genotoxic effect of PCP has been comprehensively investigated, there is little known about TCBQ’s genotoxic effects. In the current study, TCBQ was tested for its genotoxicity using HepG2 cells as experimental model. To select the exposure concentration of interest, cell viability was measured and three concentrations were used for further investigation. In single cell gel electrophoresis (SCGE) assay, concentration-dependent increase in tail length, tail DNA percentage and tail moment were detected following TCBQ exposure. Micronucleus (MN) assay indicated TCBQ gradually increased MN frequency and decreased nuclear division index (NDI). Enzyme-linked immunosorbent assay (ELISA) and western blotting analyses both showed TCBQ caused histone H2AX phosphorylation (γ-H2AX). Furthermore, the elevation of 8-hydroxydeoxyguanosine (8-OHdG) and reactive oxygen species (ROS) level indicated TCBQ-induced genotoxicity is associated with oxidative stress. On the other hand, N-acetyl-cysteine (NAC) administration significantly protected cells from the genotoxic effect of TCBQ. Overall, our data suggested TCBQ exerted genotoxic effect possibly via an oxidative damage mechanism in HepG2 cells and this toxicity is prevented by pretreatment with NAC.
8-Epidiosbulbin E acetate (EEA), a furan-containing diterpenoid lactone , is one of main component of Dioscorea bulbifera L. (DBL). It has been reported that EEA induces severe hepatotoxicity in mice and that its hepatotoxicity is associated with metabolic activation. The present study demonstrated that exposure to EEA (50, 100 or 200 μM) induced DNA damage, including significant DNA fragmentation, increases of tail DNA and olive tail moment, H2AX phosphorylation and PARP-1 activation, in cultured mouse primary hepatocytes. Similar observation was obtained in mice administered EEA at 50, 100 or 200 mg/kg. Pre-treatment with 10 μM ketoconazole (KTC), 200 μM vitamin C (VC), or 200 μM glutathione ethyl ester (GSH-OEt) reversed the over-production of reactive oxygen species (ROS) induced by EEA and attenuated susceptibility of hepatocytes to EEA-induced cytotoxicity and DNA damage in mouse primary hepatocytes. In contrast, pre-treatment with 1.0 mM L-buthionine sulfoximine (BSO) potentiated over-production of ROS, cytotoxicity and DNA damage induced by EEA. In summary, EEA induced DNA damage in cultured primary hepatocytes and the liver of mice. ROS, possibly along with DNA alkylation , participated in the observed DNA damage.
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