There is increasing evidence of activities of chlorinated by-products of bisphenol A (BPA) on retinoic acid system. Their agonistic and antagonistic activities to human retinoid X receptor (RXR) were assessed by a two-hybrid yeast assay. Aqueous solutions of 1 mg/L BPA were chlorinated by sodium hypochlorite (NaClO). It showed that chlorination of BPA increased RXR beta antagonistic activity, while no agonistic activity was detected, showing chlorine might act as a toxic potentiator rather than a toxic deactivator in RXR beta disrupting effects. BPA and its byproducts including 2,2',6,6'-tetrachlorobisphenol A (TCBPA) and 2,4,6-trichlorophenol (TCP) were quantitatively determined by gas chromatography/mass spectrometry (GC/MS). BPA rapidly degraded. With the increasing of ICC and reaction time, concentration of formed TCBPA increased initially then decreased, while concentration of formed TCP increased stably. Using the toxic equivalent (TEQ) approach, the, main contributors should be mono-, di- and tri- chlorobisphenol A at initial chlorine concentration (ICC) of 1 mg/L. At ICC of 2 and 5 mg/L, the main contributors were TCBPA and TCP, being 57.7%-70.7% and 45.3%-59.4%. Molecular docking showed BPA chlorination by-products might have the same mode of action with BPA, forming hydrogen bond and pi-pi interaction with their OH group or hydrophobic ring. (C) 2016 Elsevier B.V. All rights reserved.