Fielden M R, Chen I, Chittim B, Safe S H, Zacharewski T R
Department of Pharmacology and Toxicology, University of Western Ontario, London, Ontario, Canada.
Environ Health Perspect. 1997 Nov;105(11):1238-48. doi: 10.1289/ehp.971051238.
Several studies have reported that polychlorinated biphenyls (PCBs) exhibit estrogenic activity; however, it is not clear if these responses are associated with the polychlorinated hydrocarbon or its hydroxylated metabolite. In order to further test this hypothesis, a battery of in vitro and in vivo assays were used to investigate the estrogenic and antiestrogenic activities of 2,4,6,2',6'-pentachlorobiphenyl (PCB 104), its para-hydroxylated derivative 2,4,6,2',6'-pentachloro-4-biphenylol (HO-PCB 104), and its para-chlorinated derivative 2,4,6,2',4',6'-hexachlorobiphenyl (PCB 155). PCB 104 was found to 1) compete with tritiated 17beta-estradiol (E2) for binding to the mouse uterine estrogen receptor (ER); 2) induce gene expression in MCF-7 human breast cancer cells transiently transfected with the Gal4-human ER chimeric construct (Gal4-HEGO) and the Gal4-regulated luciferase reporter gene (17m5-G-Luc); and 3) increase MCF-7 cell proliferation in a dose-dependent manner. HO-PCB 104 exhibited greater estrogenic activity than PCB 104 in the in vitro assays examined. However, gas chromatographic-mass spectrophotometric analysis of extracts prepared from MCF-7 cells incubated with PCB 104 failed to detect the presence of the expected major metabolite HO-PCB 104. The estrogenic activity of the para-chlorinated derivative, PCB 155, was minimal compared to PCB 104 and HO-PCB 104, but it did exhibit significant antiestrogenic activity following co-treatment with 1 nM E2. Co-treatment of PCB 104 with 1 nM E2 had no effect on reporter gene expression compared to E2 alone, while 10 microM HO-PCB 104 exhibited additivity with 1 nM E2. At a dose of 202 mg/kg,PCB 104 increased uterine wet weight in ovariectomized CD-1 mice and induced vaginal epithelial cell cornification at 202, 16, and 1.7 mg/kg in a dose-dependent manner. These studies demonstrate that in addition to the hydroxylated metabolites, selected parent PCB congeners may also exhibit estrogenic and antiestrogenic activities.
多项研究报告称,多氯联苯(PCBs)具有雌激素活性;然而,尚不清楚这些反应是否与多氯代烃或其羟基化代谢产物有关。为了进一步验证这一假设,采用了一系列体外和体内试验来研究2,4,6,2',6'-五氯联苯(PCB 104)、其对羟基化衍生物2,4,6,2',6'-五氯-4-联苯酚(HO-PCB 104)及其对氯化衍生物2,4,6,2',4',6'-六氯联苯(PCB 155)的雌激素活性和抗雌激素活性。研究发现,PCB 104能够:1)与氚化17β-雌二醇(E2)竞争结合小鼠子宫雌激素受体(ER);2)在瞬时转染了Gal4-人ER嵌合构建体(Gal4-HEGO)和Gal4调控的荧光素酶报告基因(17m5-G-Luc)的MCF-7人乳腺癌细胞中诱导基因表达;3)以剂量依赖方式增加MCF-7细胞增殖。在所检测的体外试验中,HO-PCB 104表现出比PCB 104更强的雌激素活性。然而,对用PCB 104孵育的MCF-7细胞提取物进行气相色谱-质谱分析,未能检测到预期的主要代谢产物HO-PCB 104的存在。与PCB 104和HO-PCB 104相比,对氯化衍生物PCB 155的雌激素活性最小,但在与1 nM E2共同处理后,它确实表现出显著的抗雌激素活性。与单独使用E2相比,PCB 104与1 nM E2共同处理对报告基因表达没有影响,而10 μM HO-PCB 104与1 nM E2表现出相加作用。在剂量为202 mg/kg时,PCB 104增加了去卵巢CD-1小鼠的子宫湿重,并在202、16和1.7 mg/kg剂量下以剂量依赖方式诱导阴道上皮细胞角化。这些研究表明,除了羟基化代谢产物外,某些母体PCB同系物也可能表现出雌激素活性和抗雌激素活性。