The ability of four catechol estrogens of 17beta-estradiol and estrone to induce DNA adducts in Syrian hamster embryo fibroblasts.
The ability of four catechol estrogens of 17beta-estradiol and estrone to induce DNA adducts in Syrian hamster embryo fibroblasts.
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17β-雌二醇和雌酮四种儿茶酚雌激素在叙利亚仓鼠胚胎成纤维细胞中诱导 DNA 加合物的能力。
DOI：
10.1093/carcin/22.9.1505
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发表时间：
2001
期刊：
影响因子：
4.7
通讯作者：
T. Tsutsui
中科院分区：
文献类型：
--
作者：
Eiichi Yagi;J. Barrett;T. Tsutsui
儿茶酚类雌激素被认为是雌激素诱导癌变的关键中间体。我们之前已经证明，17β -雌二醇（E(2)）、雌酮（E(1)）和它们的四种儿茶酚雌激素，2-和4-羟基雌酮（2-和4-OHE(2)），以及2-和4-羟基雌酮（2-和4-OHE(1)）诱导叙利亚仓鼠胚胎（SHE）成纤维细胞的形态转化，转化能力如下：4-OHE(1) > 2- ohe (1) > 4-OHE(2) > 2- ohe(2)垂直线E(2)， E(1)。为了研究儿茶酚雌激素在激素癌变起始中的作用，我们研究了E(2)、E(1)及其儿茶酚雌激素在SHE细胞中诱导DNA加合物的能力，采用（32）p标记后实验。在浓度为10微克/毫升的儿茶酚雌激素处理1小时及以上的细胞中检测到DNA加合物。2-或4-OHE(2)形成一个单一的DNA加合物，在色谱上彼此不同。相反，2-或4-OHE(1)产生一个主要加合物和一个次要加合物，每种儿茶酚雌激素形成的两种加合物在色谱上表现出相同的流动性。浓度高达30微克/毫升的E(2)和E(1)都不能诱导DNA加合物。雌激素诱导DNA加合物的能力排序为：4-OHE(1) > 2- ohe (1) > 4-OHE(2) > 2- ohe (2) > > E(2)， E(1)，这与雌激素的转化和致癌能力很好地对应。此外，与抗氧化剂l -抗坏血酸共处理细胞后，儿茶酚类雌激素诱导的DNA加合物水平明显降低。结果表明，儿茶酚类雌激素E(2)和E(1)的氧化代谢物可能参与了内源性雌激素诱导的癌变的启动。
Catechol estrogens are considered critical intermediates in estrogen-induced carcinogenesis. We demonstrated previously that 17beta-estradiol (E(2)), estrone (E(1)) and four of their catechol estrogens, 2- and 4-hydroxyestradiols (2- and 4-OHE(2)), and 2- and 4-hydroxyestrones (2- and 4-OHE(1)) induce morphological transformation in Syrian hamster embryo (SHE) fibroblasts, and the transforming abilities vary as follows: 4-OHE(1) > 2-OHE(1) > 4-OHE(2) > 2-OHE(2) vertical line E(2), E(1). To examine the involvement of catechol estrogens in the initiation of hormonal carcinogenesis, we studied the ability of E(2), E(1) and their catechol estrogens to induce DNA adducts in SHE cells by using a (32)P-post-labeling assay. DNA adducts were detected in cells treated with each of all the catechol estrogens at concentrations of 10 microg/ml for 1 h and more. 2- or 4-OHE(2) formed a single DNA adduct, which was chromatographically distinct from each other. In contrast, 2- or 4-OHE(1) produced one major and one minor adduct, and the two adducts formed by each catechol estrogen exhibited identical mobilities on the chromatograms. Neither E(2) nor E(1) at concentrations up to 30 microg/ml induced DNA adducts. The abilities of the estrogens to induce DNA adducts were ranked as follows: 4-OHE(1) > 2-OHE(1) > 4-OHE(2) > 2-OHE(2) > > E(2), E(1), which corresponds well to the transforming and carcinogenic abilities of the estrogens. In addition, the level of DNA adducts induced by the catechol estrogens was markedly decreased by co-treatment of cells with the antioxidant L-ascorbic acid. The results indicate the possible involvement of oxidative metabolites of catechol estrogens of E(2) and E(1) in the initiation of endogenous estrogen-induced carcinogenesis.
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维生素 C 对叙利亚仓鼠雌激素诱导的肾癌的抑制作用。
影响因子：
11.2
作者：
Liehr,JG;Wheeler,WJ
通讯作者：
Wheeler,WJ
己烯雌酚诱发癌变之前的靶器官特异性共价 DNA 损伤。
影响因子：
4.7
作者：
Liehr,JG;Randerath,K;Randerath,E
通讯作者：
Randerath,E
仓鼠肾微粒体提高雌二醇的 4-羟基化：雌激素代谢激活的潜在途径。
影响因子：
4.8
作者：
Weisz,J;Bui,QD;Roy,D;Liehr,JG
通讯作者：
Liehr,JG
DOI：
10.1016/0022-4731(86)90080-4
发表时间：
1986-01-01
影响因子：
4.1
作者：
LIEHR, JG;FANG, WF;ARIULUBELEN, A
通讯作者：
ARIULUBELEN, A
影响因子：
4.1
作者：
Stack, DE;Byun, J;Cavalieri, EL
通讯作者：
Cavalieri, EL