https://www.selleckchem.com/products/hsp27-inhibitor-j2.html The presence of NO3- promoted RhB degradation, while H2PO4- and C2O42- showed an inhibitory effect on both UV/H2O2 and UV/PS processes. Radical scavenging tests revealed the dominant role of SO4•- radicals in the UV/PS system. Furthermore, the evolution of low molecular weight organic acids and NH4+ during the degradation of RhB in these two processes were compared. Both UV/H2O2 and UV/PS systems led to similar formation trends of NH4+ and some ring-opening products (e.g., formic acid, acetic acid, and oxalic acid), suggesting some analogies in the decay pathways of RhB by •OH and SO4•--induced oxidation processes. Novel brominated flame retardants (NBFRs) have been widely used and frequently detected in various environmental matrices. In this study, 2-ethylhexyl-2,3,4,5-tetrabromobenzoate (TBB), bis-(2-ethylhexyl) tetrabromophthalate (TBPH) and their metabolites (namely 2,3,4,5-tetra-bromo benzoic acid (TBBA) and mono(2-ethylhexyl) tetrabromophthalate (TBMEHP)) were exposed to human umbilical vein endothelial cells (HUVECs). Metabolites can induce stronger cytotoxicity than parent compounds with EC50 at 47.3 (TBBA), 8.6 μg/ml (TBMEHP) vs > 200 μg/mL for parent compounds. Gene expression of platelet endothelial cell adhesion molecule-1, the gene associated with blood platelet kinetics, was significantly induced under TBBA and TBMEHP exposure. The in vivo test was consistent with gene expression result that the number of platelets in mouse blood was significantly increased after gavaged with 0.8 μg/mL TBBA and TBMEHP. In addition, TBB or TBPH were exposed to mice via gavage, and higher concentrations of TBBA (4 h, 60.8 ± 12.9 ng/mL, 8 h, 69.4 ± 2.24 ng/mL) in mouse blood were found than those of TBMEHP (4 h, 17.2 ± 4.01 ng/mL, 8 h, 12.8 ± 3.20 ng/mL), indicating that TBB was more readily in vivo metabolized than TBPH. The in vivo metabolism of TBB and TBPH and the stronger toxicity of their metabolites unde