Plasma concentrations of pituitary hormones in 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated male rats.
Plasma concentrations of pituitary hormones in 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated male rats.
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2,3,7,8-四氯二苯并-对-二恶英治疗的雄性大鼠中垂体激素的血浆浓度。
DOI：
10.1002/jbt.2570040305
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Peterson,RE
中科院分区：
文献类型：
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作者：
Moore,RW;Parsons,JA;Bookstaff,RC;Peterson,RE
进行实验是为了检验急性 TCDD 毒性与垂体功能减退相关的假设。性成熟的雄性 Sprague-Dawley 大鼠被给予分级剂量的 TCDD（0-100 μg/kg），并在 7 天后进行评估。尽管有明显的吞咽不足和体重减轻，但任何剂量的 TCDD 均不会显着影响生长激素 (GH)、卵泡刺激素 (FSH) 和黄体生成素 (LH) 的血浆浓度。仅催乳素（PRL）浓度降低，而正如之前报道的那样，促甲状腺激素浓度升高。此外，单剂量 TCDD（50 μg/kg）后 1、2、3、4、5 或 7 天后，血浆 LH、PRL 和促肾上腺皮质激素 (ACTH) 浓度没有受到显着影响。我们的结论是：（1）垂体功能减退不是急性 TCDD 毒性初始阶段的主要原因，（2）TCDD 治疗大鼠的生长迟缓不是 GH 缺乏的结果，（3）血浆皮质酮浓度的变化是由于肾上腺对 ACTH 刺激的反应性改变而不是血浆 ACTH 浓度的变化，（4）精子发生受损与血浆 FSH 浓度降低无关。此外，对血浆 PRL 浓度缺乏一致的影响表明，血浆 PRL 浓度的变化在 TCDD 的毒性中并不起关键作用。最后，由于 TCDD 治疗会导致严重的雄激素缺乏，但不会增加雄激素分解代谢或排泄的速率，因此血浆 LH 浓度不受影响的事实表明 TCDD 治疗必须降低睾丸对 LH 刺激的反应性。此外，由于不存在对低血浆雄激素浓度（血浆 LH 浓度显着升高）的预期补偿反应，这些观察结果还表明 TCDD 治疗必定会干扰血浆 LH 浓度的调节。
Experiments were conducted to test the hypothesis that acute TCDD toxicity is associated with pituitary hypofunction. Sexually mature male Sprague‐Dawley rats were given graded doses of TCDD (0–100 μg/kg) and evaluated 7 days later. Despite pronounced hypophagia and body weight loss, plasma concentrations of growth hormone (GH), follicle‐stimulating hormone (FSH), and luteinizing hormone (LH) were not significantly affected by any dose of TCDD. Only prolactin (PRL) concentrations were reduced, while, as previously reported, thyroid‐stimulating hormone concentrations were elevated. Also, plasma LH, PRL, and adrenocorticotropic hormone (ACTH) concentrations were not significantly affected 1, 2, 3, 4, 5, or 7 days after a single dose of TCDD (50 μg/kg). We conclude that (1) pituitary hypofunction is not a major cause of the initial stages of acute TCDD toxicity, (2) growth retardation in TCDD‐treated rats is not the result of a deficiency of GH, (3) alterations in plasma corticosterone concentrations are due to altered responsiveness of the adrenal to ACTH stimulation rather than to changes in plasma ACTH concentrations, and (4) that impaired spermatogenesis is not associated with a decrease in plasma FSH concentrations. In addition, the lack of a consistent effect on plasma PRL concentrations suggests that alterations in plasma PRL concentrations do not play a critical role in the toxicity of TCDD. Finally, because TCDD treatment causes a serious androgenic deficiency without increasing the rates at which androgens are catabolized or excreted, the fact that plasma LH concentrations were unaffected indicates that TCDD treatment must reduce the responsiveness of the testis to LH stimulation. In addition, because the expected compensatory response to low plasma androgen concentrations (a pronounced elevation in plasma LH concentrations) was absent, these observations also indicate that TCDD treatment must interfere with the regulation of plasma LH concentrations.