摘要
目的探讨乙炔基雌二醇(EE)投药及不投药的情况下,内源性雄性激素对二甲基氨基苯甲醛(DMAB)并用丙酸睾丸酮(TP)或双氢睾酮(DHT)而诱发的大鼠前列腺癌发病过程中的作用机制。方法为排除内源性雄性激素对实验结果的干扰,F344大鼠在投入DMAB诱发前列腺癌后立即予以去势,然后分为TP投药组、DHT投药组、TP/EE并用组及DHT/EE并用组,投药时间为40周。结果DMAB与TP的并用增加了前列腺前部、侧部及精囊的浸润性癌肿的发生,而双氢睾酮并没有表现出相同的作用。同样在DMAB与丙酸睾丸酮/乙炔基雌二醇(TP/EE)并用组,前列腺、精囊浸润性癌的发生率明显增高,而在DMAB与或双氢睾酮(DHT)/乙炔基雌二醇(TP/EE)并用组则无明显变化。另外,除了在单纯DMAB投药的去势的大鼠组以外,其他各组均产生了癌变,这个结果与此前已报告的在未去势大鼠中的实验结果十分相近。结论内源性的睾酮对TP/EE及DMAB并用而诱发的前列腺癌无明显影响,同时也不参与DHT的作用机制。
Objective To explore the effect of endogenous androgen on rat nrostatecarcinoeenesis induced by 3,2'-dimethyl-4-aminobiphenyl (DMAB) and testosterone orooionate(TP) or 5α-dihydrotestosterone (DHT) with or without ethinyl estradiol (EE).MethodsInorder to eliminate the influence of endogenous androgen, F344 rats were orchiectomized justafter initiation with the prostate carcinogen, DMAB, and then given TP, DHT, TP plusEE or DHT olus EE for 40 weeks.ResultsThe results demonstrated that while administrationof TP following DMAB treatment causes invasive carcinomas in the lateral and anterior Drostateand seminal vesicles, DHT does not exhibit eauivalent effects. Synergistic enhancement was alsoevident with TP olus EE, but not with DHT olus EE. The incidences of orostatic and seminalvesicle lesions in all groups of the oresent experiment. except for the group eiven castrationwithout hormonal supplement, were equivalent to those previously found in non-castratedanimals.ConclusionTherefore, the present findings indicate that endogenous testosteronemay not be reauired for oromotion by TP/EE of DMAB?initiated orostate carcinogenesis andthat it may not contribute to the actions of DHT.[
出处
《罕少疾病杂志》
2004年第3期31-34,52,共5页
Journal of Rare and Uncommon Diseases
