International Journal of Environmental Research and Public Health   2016 年 13 卷 2 期

2016.01.26

Arsenic is ubiquitously present in human lives, including in the environment and organisms, and has divergent effects between different cells and tissues and between different exposure times and doses. These observe defects have been attributed to the nuclear transcription factor kappa B(NF-??B) signaling pathway. Herein, a meta-analysis was performed by independently searching databases including the Cochrane Library, PubMed, Springer, Embase, and China National Knowledge Infrastructure, to analyze effects of arsenic exposure on NF-??B signaling. Compared to controls, in the exposed group, p-I??B levels were found to be 8.13-fold higher (95% CI, 2.40??“13.85; Z = 2.78; p = 0.005),I??Blevelswere16.19-foldlower(95%CI,??27.44??“??4.94;Z=2.78;p=0.005),andNF-??Bp65 levels were 0.77-fold higher (95% CI, 0.13??“1.42; Z = 2.34; p = 0.02) for normal cells and tissue, while NF-??Bp65 levels were 4.90-fold lower (95% CI,??8.49??“1.31; Z = 2.62; p = 0.009), NF-??B activity was 2.45-fold lower (95% CI,??3.66??“1.25; Z = 4.00; p < 0.0001), and DNA-binding activity of NF-??B was 9.75-fold lower (95% CI,??18.66??“4.54; Z = 2.15; p = 0.03) for abnormal cells and tissue. Short exposure to high arsenic doses activated the NF-??B signaling pathway, while long exposure to low arsenic doses suppressed NF-??B signaling pathway activation. These ???ndings may provide a theoretical basis for injurious and therapeutic mechanisms of divergent effects of arsenic.