Induction of apoptosis by UV-irradiated chlorinated bisphenol A in Jurkat cells
Induction of apoptosis by UV-irradiated chlorinated bisphenol A in Jurkat cells
复制标题
DOI：
10.1016/j.tiv.2008.01.001
复制
发表时间：
2008-06-01
影响因子：
3.2
通讯作者：
Goto, Rensuke
中科院分区：
文献类型：
--
作者：
Mutou, Yasuko;Ibuki, Yuko;Goto, Rensuke
在废纸回收厂废水中检测到氯代双酚A （ClBPAs）。我们之前报道了双酚A （BPA）和clbpa[3-氯双酚A， 3,3'-二氯双酚A和3,3'，5-三氯双酚A]在紫外线（UV） B或UVC（而不是UVA）照射下诱导细胞生长抑制，并且在光产物中检测到3-羟基双酚A (3- ohbpa) [Mutou， Y., Ibuki， Y., Terao， Y., Kojima， S., Goto， R., 2006]。紫外线照射下氯代双酚A的化学变化及其产物对Jurkat细胞的细胞毒性。环境毒理学杂志，2002,28(3):391 - 391。紫外线照射形成羟基化双酚a可能对细胞生长有抑制作用，但其抑制生长的机制尚不清楚。在本研究中，我们研究了暴露于UVA、UVB或UVC的BPA、clbpa和3-OHBPA是否能诱导Jurkat细胞死亡，以及细胞死亡的模式是否为凋亡。暴露于UVB和UVC的clbpa诱导了显著的细胞死亡，而暴露于UVA和BPA的clbpa则没有。细胞凋亡是由于染色质凝结和DNA断裂引起的。caspase-3、-8和-9的激活以及细胞色素c的释放表明，暴露于UVB或UVC的cibpa通过典型的凋亡途径诱导凋亡。此外，3-OHBPA诱导的细胞凋亡与UVB或uvc辐照的ClBPA相似。这些结果表明，紫外光照射产生的CIBPAs光产物含有3-OHBPA，有助于诱导细胞凋亡。(c) 2008 Elsevier Ltd.版权所有。
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, 283289]. 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 CIBPAs 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 CIBPAs generated by UV irradiation, containing 3-OHBPA, contributed to the induction of apoptosis. (c) 2008 Elsevier Ltd. All rights reserved.