title: Induction of apoptosis by UV-irradiated chlorinated bisphenol A in Jurkat cells.
abstract: Chlorinated derivatives of bisphenol A (ClBPAs) have been detected in wastewater from waste paper recycling plants. We previously reported that bisphenol A (BPA) and ClBPAs [3-chlorobisphenol A, 3,3'-dichlorobisphenol A, and 3,3',5-trichlorobisphenol A] irradiated with ultraviolet (UV) B or UVC (not with UVA) induced inhibition of cell growth, and that 3-hydroxybisphenol A (3-OHBPA) was detected in the photoproducts [Mutou, Y., Ibuki, Y., Terao, Y., Kojima, S., Goto, R., 2006b. Chemical change of chlorinated bisphenol A by ultraviolet irradiation and cytotoxicity of their products on Jurkat cells. Environmental Toxicology and Pharmacology, 21, 283-289]. The formation of hydroxylated BPAs by UV irradiation might contribute to the inhibition of cell growth, but the mechanism of the growth inhibition is not clarified. In this study, we investigated whether BPA and ClBPAs exposed to UVA, UVB, or UVC, and 3-OHBPA could induce the death of Jurkat cells and whether the pattern of cell death was apoptosis. ClBPAs exposed to UVB and UVC induced significant cell death, but those exposed to UVA and BPA did not. The cell death was apoptosis because chromatin condensation and DNA fragmentation were detected. Activation of caspase-3, -8, and -9 and cytochrome c release indicated that ClBPAs exposed to UVB or UVC induced apoptosis via typical apoptotic pathways. In addition, 3-OHBPA induced apoptosis similar to UVB- or UVC-irradiated ClBPA. These results suggested that the photoproducts of ClBPAs generated by UV irradiation, containing 3-OHBPA, contributed to the induction of apoptosis.
authors.affiliation: Laboratory of Radiation Biology, Graduate School of Nutritional and Environmental Sciences, University of Shizuoka, 52-1 Yada, Shizuoka-shi 422-8526, Japan.
authors.forename: Yasuko
authors.initials: Y
authors.lastname: Mutou
authors.forename: Yuko
authors.initials: Y
authors.lastname: Ibuki
authors.forename: Yoshiyasu
authors.initials: Y
authors.lastname: Terao
authors.forename: Shuji
authors.initials: S
authors.lastname: Kojima
authors.forename: Rensuke
authors.initials: R
authors.lastname: Goto
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D001559:Benzhydryl Compounds; D053148:Caspase 3 / Q000187:drug effects / Q000378:metabolism; D053181:Caspase 8 / Q000187:drug effects / Q000378:metabolism; D053453:Caspase 9 / Q000187:drug effects / Q000378:metabolism; D017606:Chlorine Compounds / Q000737:chemistry / Q000633:toxicity*; D002843:Chromatin / Q000187:drug effects / Q000378:metabolism; D045304:Cytochromes c / Q000187:drug effects / Q000378:metabolism; D053938:DNA Fragmentation / Q000187:drug effects; D006801:Humans; D019169:Jurkat Cells / Q000187:drug effects / Q000378:metabolism; D010636:Phenols / Q000737:chemistry / Q000633:toxicity*; D014466:Ultraviolet Rays; D014874:Water Pollutants, Chemical / Q000737:chemistry / Q000633:toxicity; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D053148:Caspase 3; D053181:Caspase 8; D053453:Caspase 9; D017606:Chlorine Compounds; D002843:Chromatin; D045304:Cytochromes c; D010636:Phenols; D014874:Water Pollutants, Chemical; C530259:3-hydroxybisphenol A; C006780:bisphenol A; D000098826:Bisphenol A Compounds