Section of Radiation Biology, Faculty of Life Sciences, University of Vienna, Althanstr. 14, UZA II, A-1090 Vienna, Austria.
In Vivo. 2010 Jul-Aug;24(4):535-41.
Based on the different behaviour of 17beta-estradiol (17betaE(2)) and progesterone (PRG), it was of interest to investigate the interaction of both hormones in respect of their electron emission and cytotoxicity by experiments in vitro.
The studies include determination of emitted electrons (e(-)(aq)) by the individual hormones as well as by their mixtures, all complexed with cyclodextrin (HBC). Experiments in vitro (Escherichia coli bacteria) were performed for a better understanding of the mechanisms involved. Survival ratios, DeltaD(37)(Gy), were calculated.
Aqueous HBC as well as 17betaE(2) and PRG, individually as well as in mixtures, are able to emit e(-)(aq). The resulting transients can lead to the formation of metabolites, some of which can initiate cancer. It was established that both hormones, 17betaE(2) and PRG, interact in respect to their electron emission property. In the frame of experiments in vitro, it was found that oxidizing radicals (OH, O(2)(-)) lead to negative DeltaD(37)(Gy) values, indicating cytostatic properties. On the other hand, the primary reducing radicals (e(-)(aq), H) lead to positive DeltaD(37)(Gy) values, indicating a radical-scavenging effect.
The main outcome of this work is that PRG in combination with 17betaE(2) can strongly reduce the number of carcinogenic 17betaE(2)-metabolites. This fact offers a new pathway for application of hormones in medical treatment of patients.
基于 17β-雌二醇(17βE(2))和孕酮(PRG)的不同行为,我们有兴趣研究这两种激素在与环糊精(HBC)络合时,在其电子发射和细胞毒性方面的相互作用。
研究包括单独以及混合时的激素所发射的电子(e(-)(aq))的测定,以及它们的混合物,所有的都与环糊精(HBC)络合。体外实验(大肠杆菌细菌)的进行是为了更好地理解所涉及的机制。计算了存活比,DeltaD(37)(Gy)。
HBC 水溶液以及 17βE(2)和 PRG 单独以及混合物都能够发射 e(-)(aq)。由此产生的瞬变可以导致代谢物的形成,其中一些可以引发癌症。结果表明,这两种激素,17βE(2)和 PRG,在电子发射特性方面相互作用。在体外实验中,发现氧化自由基(OH、O(2)(-))导致负的 DeltaD(37)(Gy)值,表明具有细胞抑制特性。另一方面,原始还原自由基(e(-)(aq)、H)导致正的 DeltaD(37)(Gy)值,表明具有自由基清除作用。
这项工作的主要结果是,PRG 与 17βE(2)联合使用可以大大减少致癌的 17βE(2)代谢物的数量。这一事实为激素在患者的医疗治疗中的应用提供了一条新途径。