An endocrine disruptor, bisphenol-A (BPA), has been reported to have several short-term actions in various cells and tissues. However, the mechanisms of these actions have not been fully elucidated. In order to assess the effect of BPA on the intercellular communication modiated by gap junctions, we conducted the present study in the rat epithelium-derived BICR-M1Rk cell-line, in which connexin 43 (Cx43) is a major gap junction channel-forming protein. The cytotoxicity of BPA toward the cultured cells was evaluated by using both MTT reduction and LDH leakage assay systems. The results showed no appreciable loss in cell viability in the presence of increasing concentrations of BPA (from 0.1 to 3.2 ${mu}$M) for 1 h incubation. However, most of cell viability was lost when cells were incubated for 24 hr with the same concen-trations of BPA. The BPA acted as an antagonist on gap junction-mediated intercellular communication (GJIC), and the phenomenon was dose-dependent and irreversible. Accord-ing to the data obtained from scrape-leading dye-transfer experiments, three quarters of nor-mal GJIC was reduced by concentration of 0.4 ${mu}$M BPA for 1 h incubation. To identify there levance of this retardation upon BPA treatment, the GJIC to Cx43 synthesis, the mRNA and protein levels of Cx43 were assessed with RT-PCR and Western-blotting, respectively. The total protein level of Cx43 was almost constant in a wide range of BPA concentrations, as wel las in Cx43 mRNA level. These results suggest that BPA inhibits GJIC through a modulation of the gating of gap junction channels, not through a genomic modulation of Cx43.