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Perchlorate and chlorate are both strong oxidants and thyroid toxicants that are widely distributed in soil, water and human foods. The red swamp crayfish (Procambarus clarkii) is a common aquatic organism that is popular in Chinese culinary dishes. Dietary intake is the main route of human exposure to perchlorate and chlorate, though the health risks of crayfish consumption are unknown. Thus, this study investigated the quantities of perchlorate and chlorate in red swap crayfish from sampling sites in five provinces located near the Yangtze River in China, along with the associated health risks of consuming this species. Perchlorate was detected in 55.6-100 % of crayfish samples in each sampling location, and chlorate was found in 100 % of samples cross all sites. Concentrations of perchlorate in crayfish from upstream provinces (Hubei, Hunan and Jiangxi) were higher than those from downstream provinces (Anhui and Jiangsu). Perchlorate and chlorate concentrations were positively correlated in crayfish, suggesting that chlorate may be a degradation byproduct of perchlorate. The quantities of both pollutants in hepatopancreas tissue were higher than in muscle tissues (p0.05), such that we do not recommend ingesting crayfish hepatopancreas. Hazard quotient (HQ) values for chlorate in crayfish were1 across all provinces, suggesting no potential health risk of chlorate exposure through crayfish consumption. However, perchlorate concentrations in crayfish from the Jiangxi province had an associated HQ value1, suggesting potential risks for human health. These results will be useful in informing mitigation measures aimed at reducing perchlorate exposure associated with crayfish consumption.

Hydroquinone (HQ), one of the major metabolites of benzene, can induce aberrant gene expression. MiR-155, a tumor activator, participates in various biological processes, including DNA damage response. However, the molecular mechanism of aberrant miR-155 expression is still not completely elucidated. Here, we investigated the mechanism of abnormal expression of miR-155 induced by poly(ADP-ribose)polymerase-1 (PARP-1) expression in HQ-treated TK6 lymphoblastoid cells. We examined the expression of genes related to abnormal expression of miR-155 to explore the reason for this phenomenon. The results of the present study showed that miR-155 was significantly increased and reactive oxygen species (ROS) were decreased in cells treated with HQ for 72 h compared with PBS-treated cells. Meanwhile, E4F1, PARP-1 and PARP-1 related co-regulators (NF-κB, HDAC1, and HDAC2), acetylated histone H3 (H3Ac) were increased in a concentration-dependent manner. Experiments for treatment with 5-AzaC (DNMTs inhibitor), TSA (HDACs inhibitor), DOX (to activate PARP-1) or MG132 (proteasome inhibitor) revealed that the MBDs and PARP-1 was positively associated with miR-155 expression. Moreover, in cells treated with HQ in conjunction with PARP-1 knockdown, expression of miR-155, H3Ac and MBD2 protein were decreased, compared with negative control. In conclusion, PARP-1 activates expression of miR-155 via acetylation by regulating MBD2 in TK6 cells exposed to HQ.