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首页> 外文期刊>Reproductive toxicology >Alteration in ovarian gene expression in response to 2,3,7,8-tetrachlorodibenzo-p-dioxin: reduction of cyclooxygenase-2 in the blockage of ovulation.
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Alteration in ovarian gene expression in response to 2,3,7,8-tetrachlorodibenzo-p-dioxin: reduction of cyclooxygenase-2 in the blockage of ovulation.

机译：响应2、3、7、8-四氯二苯并-p-二恶英而改变卵巢基因表达：减少排卵中的环氧合酶2含量。

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a reproductive toxicant and endocrine disrupter that is known to block ovulation. This study was designed to investigate alterations in relevant ovarian genes that may be involved in the blockage of ovulation by TCDD in immature intact rats primed with equine chorionic gonadotropin (eCG). In this ovulation model, rats were given either 32&mgr;g/kg TCDD or corn oil by gavage on 25days of age. The next day, eCG (5IU) was injected subcutaneously (s.c.) to stimulate follicular development. Ovulation occurs 72h after administration of eCG in controls of this model. TCDD blocked ovulation at the expected time and also reduced both ovarian and body weights. At 72h after eCG (the morning after expected ovulation), TCDD did not alter significantly serum concentrations of progesterone (P4) and androstenedione (A4). However, estradiol (E2) was significantly higher at 72h after eCG in TCDD-treated rats when compared with controls. Western blots revealed that ovarian CYP1A1 was induced by TCDD. In addition, the aryl hydrocarbon receptor (AhR) and AhR nuclear translocator (ARNT) were down- and up-regulated by TCDD, respectively, indicating that AhR-mediated signal transduction was altered in the ovary. Ovarian estrogen receptor (ER)alpha, ERbeta and progesterone receptor (PR) were not altered significantly by TCDD, but ovarian glucocorticoid receptor (GR) was increased at 24h after TCDD and decreased at 72h after eCG when compared with controls. TCDD induced the early appearance of ovarian plasminogen activator inhibitor type-1 (PAI-1), plasminogen activator inhibitor type-2 (PAI-2), urokinase plasminogen activator (uPA), and tissue plasminogen activator (tPA) at 24h after dosing when compared with controls. On the morning after ovulation (72h after eCG), no significant differences between control and TCDD-treated rats were observed except that TCDD had still increased tPA and decreased PAI-2 when compared with controls. Interestingly, ovarian COX-2 was induced on the morning after ovulation (72h after eCG) in controls, but was greatly inhibited in TCDD-treated rats at that time. On the other hand, COX-1 was constitutively expressed throughout the ovulatory period and remained unaffected by TCDD. Immunolocalization of COX-2 in the ovary revealed that TCDD inhibited COX-2 expression in the granulosa cell layer when assessed in the morning of expected ovulation. In conclusion, AhR signaling is activated in the ovary by TCDD and inhibition of COX-2 appeared to be a critical step in the TCDD blockage of ovulation because blockage or reduction of COX-2 expression is well known to be associated with failure of ovulation.
机译：2,3,7,8-四氯二苯并-对-二恶英（TCDD）是一种生殖毒性和内分泌干扰物，已知会阻止排卵。这项研究旨在调查与卵巢绒毛膜促性腺激素（eCG）交配的未成熟完整大鼠中TCDD可能影响排卵的相关卵巢基因的变化。在该排卵模型中，在25日龄时通过管饲法给大鼠施用32mg / kg TCDD或玉米油。第二天，皮下注射（皮下注射）eCG（5IU）以刺激卵泡发育。在该模型的对照中施用eCG后72小时排卵。 TCDD在预期的时间阻止了排卵，还减少了卵巢和体重。 eCG后72小时（预期排卵后的早晨），TCDD并未显着改变孕酮（P4）和雄烯二酮（A4）的血清浓度。但是，与对照组相比，TCDD治疗的大鼠在eCG后72h雌二醇（E2）显着升高。 Western印迹表明，TCDD诱导了卵巢CYP1A1的表达。此外，TCDD分别下调和上调了芳烃受体（AhR）和AhR核转运子（ARNT），表明AhR介导的信号转导在卵巢中发生了改变。与对照组相比，TCDD并未显着改变卵巢雌激素受体（ER）α，ERbeta和孕酮受体（PR），但与对照相比，TCDD后24h卵巢糖皮质激素受体（GR）升高，而eCG后72h降低。 TCDD在给药后24h时诱导卵巢纤溶酶原激活物抑制剂1型（PAI-1），纤溶酶原激活物抑制剂2型（PAI-2），尿激酶纤溶酶原激活物（uPA）和组织纤溶酶原激活物（tPA）的早期出现。与控件相比。在排卵后的早晨（eCG后72小时），对照组和TCDD处理的大鼠之间没有观察到显着差异，除了TCDD与对照组相比仍具有增加的tPA和降低的PAI-2。有趣的是，在对照中排卵后的早晨（eCG后72h）诱导了卵巢COX-2，但在当时用TCDD处理的大鼠中卵巢COX-2被大大抑制了。另一方面，COX-1在整个排卵期均组成性表达，并且不受TCDD的影响。卵巢中COX-2的免疫定位表明，当在预期排卵的早晨进行评估时，TCDD抑制了颗粒细胞层中COX-2的表达。总之，AhR信号在卵巢中被TCDD激活，抑制COX-2似乎是TCDD阻断排卵的关键步骤，因为众所周知，阻断或降低COX-2表达与排卵失败有关。

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