ANDROGENIC DEFICIENCY IN MALE-RATS TREATED WITH PERFLUORODECANOIC ACID
ANDROGENIC DEFICIENCY IN MALE-RATS TREATED WITH PERFLUORODECANOIC ACID
复制标题
DOI：
10.1016/0041-008x(90)90306-f
复制
发表时间：
1990-06-15
影响因子：
3.8
通讯作者：
PETERSON, RE
中科院分区：
文献类型：
--
作者：
BOOKSTAFF, RC;MOORE, RW;PETERSON, RE
全氟癸酸（PFDA，20-80 mg/kg ip）给药7天后，观察对性成熟雄性大鼠雄激素水平的影响。PFDA以剂量依赖性方式降低血浆雄激素浓度，ED 50约为30 mg/kg。最高剂量的PFDA降低了血浆睾酮和5 α-雌二醇水平。将双氢睾酮浓度分别降低至自由进食对照（ALC）值的12%和18%。继发于血浆雄激素浓度降低的是附属性器官重量和上皮高度的剂量相关性降低。配对喂养对照（PFC）大鼠的结果表明，PFDA处理大鼠的摄食量不足不是血浆雄激素浓度低的主要原因。当大鼠被阉割并植入含睾酮的胶囊时，PFDA处理的大鼠和ALC大鼠具有相似的血浆睾酮浓度和第二性器官重量。因此，完整PFDA处理大鼠中的雄激素缺乏不是由雄激素的血浆清除率增加引起的。相反，PFDA必须通过减少睾丸分泌睾酮来引起雄激素缺乏症。睾酮分泌的减少似乎不是由于血浆促黄体生成素（LH）浓度的降低，因为PFDA治疗未显著改变血浆LH浓度。这一发现表明PFDA治疗降低了睾丸对LH刺激的反应性。PFDA处理减少了LH类似物人绒毛膜促性腺激素体外刺激睾丸的睾酮分泌，这一观察结果证明了这一点。此外，由于血浆LH浓度没有增加，在PFDA治疗的大鼠低血浆雄激素浓度的反应，我们认为，PFDA破坏了正常的反馈关系，血浆雄激素和LH浓度之间存在。
Effects of perfluorodecanoic acid (PFDA, 20-80 mg/kg ip) on the androgenic status of sexually mature male rats were investigated 7 days after treatment. PFDA decreased plasma androgen concentrations in a dose-dependent fashion with an ED50 of approximately 30 mg/kg. The highest dose of PFDA decreased plasma testosterone and 5.alpha.-dihydrotestosterone concentrations to 12 and 18%, respectively, of ad libitum-fed control (ALC) values. Secondary to the decreased plasma androgen concentrations were dose-related decreases in the weights and epithelial heights of accessory sex organs. Results from pair-fed control (PFC) rats show that hypophagia in PFDA-treated rats was not a major cause of the low plasma androgen concentrations. When rats were castrated and implanted with testosterone-containing capules, PFDA-treated and ALC rats had similar plasma testosterone concentrations and secondary sex organ weights. Therefore, the androgenic deficiency in intact PFDA-treated rats does not result from increased plasma clearance of androgens. Rather, PFDA must cause the androgenic deficiency by decreasing the secretion of testosterone from the testis. The decrease in testosterone secretion does not appear to result from a decrease in plasma luteinizing hormone (LH) concentrations, because plasma LH concentrations were not significantly altered by PFDA treatment. This finding suggests that PFDA treatment decreases testicular responsiveness to LH stimulation. The observation that PFDA treatment reduced the secretion of testosterone by testes stimulated in vitro with the LH analog human chorionic gonadotropin demonstrates that this is the case. In addition, since plasm LH concentrations did not increase in response to the low plasma androgen concentrations in PFDA-treated rats we suggest that PFDA disrupts the normal feedback relationship which exists between plasma androgen and LH concentrations.