Umbreit T H, Hesse E J, Macdonald G J, Gallo M A
Department of Environmental and Community Medicine, University of Medicine and Dentristry of New Jersey, Robert Wood Johnson Medical School, Piscataway.
Toxicol Lett. 1988 Jan;40(1):1-9. doi: 10.1016/0378-4274(88)90177-4.
Interactions of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and estradiol were studied in three strains of mice: CD-1 and C57B/6 (TCDD sensitive) and DBA/2 (TCDD resistant at lower doses). Immature females were injected with 0-200 ng/kg/day estradiol for 2 weeks, s.c. On days 7, 9, 11, and 13, mice received 10 micrograms TCDD/kg by gavage. Relative uterine weight increased in mice of all three strains treated with estradiol alone. Uterine imbibition was suppressed by TCDD treatment, although this effect was antagonized in a saturable manner by coadministration of estradiol. TCDD induced aryl hydrocarbon hydroxylase (AHH) in liver microsomes of treated mice independent of estradiol dose and strain of mice (the dose of TCDD used was high enough to cause AHH induction in the resistant DBA/2 mice). Treatment of CD-1 mice, but not other strains, with TCDD and estradiol resulted in a decrease in the electrophoretic band of hepatic microsomal proteins comigrating with cytochrome P-450a and epoxide hydrase.
在三种品系的小鼠中研究了2,3,7,8-四氯二苯并对二恶英(TCDD)与雌二醇的相互作用:CD-1和C57B/6(对TCDD敏感)以及DBA/2(在较低剂量下对TCDD有抗性)。未成熟雌性小鼠皮下注射0 - 200 ng/kg/天的雌二醇,持续2周。在第7、9、11和13天,小鼠通过灌胃接受10微克TCDD/kg。单独用雌二醇处理的所有三个品系的小鼠子宫相对重量均增加。TCDD处理抑制了子宫吸收,尽管雌二醇的共同给药以饱和方式拮抗了这种作用。TCDD在处理过的小鼠肝脏微粒体中诱导芳烃羟化酶(AHH),与雌二醇剂量和小鼠品系无关(所用TCDD剂量足以在抗性DBA/2小鼠中引起AHH诱导)。用TCDD和雌二醇处理CD-1小鼠(而非其他品系)导致与细胞色素P-450a和环氧化物水解酶共迁移的肝脏微粒体蛋白电泳条带减少。