Raivio T, Palvimo J J, Dunkel L, Wickman S, Jänne O A
Biomedicum Helsinki, Department of Physiology, Institute of Biomedicine, University of Helsinki, FIN-00014 Helsinki, Finland.
J Clin Endocrinol Metab. 2001 Apr;86(4):1539-44. doi: 10.1210/jcem.86.4.7329.
We have developed a mammalian cell (COS-1) bioassay, which can measure androgen bioactivity directly from a small amount (10 microL) of human serum. The recombinant assay is based on androgen-dependent interaction between the ligand-binding domain and the N-terminal region of the androgen receptor (AR), which were fused to Gal4 DNA-binding domain of Saccharomyces cerevisiae and transcriptional activation domain of herpes simplex VP16 protein, respectively. The interaction is amplified by coexpression of AR-interacting protein 3 in the cells. The reporter plasmid contains 5 Gal4-binding sites upstream of the luciferase gene; luciferase activity in cell lysates is derived from androgen bioactivity in human serum. Saturating concentration of testosterone in FCS induced more than 700-fold induction in relative luciferase activity. The sensitivity was less than 1.0 nmol/L testosterone in FCS. The intra- and interassay coefficients of variation were 8.3% and 21%, respectively. Interaction between the AR termini was blocked by nonsteroidal antiandrogens, and the assay exhibited minimal cross-reactivity with 17 beta-estradiol. Serum androgen bioactivity was studied in 23 boys (13.9--16.8 yr old) with constitutional delay of puberty and in 9 prepubertal boys with cryptorchidism (1.0--6.4 yr old). Androgen bioactivity was detectable in 15 boys with constitutional delay of puberty and in all boys with cryptorchidism during treatment with human CG (range, 1.0-14.5 nmol/L testosterone equivalents). Serum androgen bioactivity measured by the bioassay correlated strongly with serum testosterone concentration (r = 0.93, P < 0.0001, n = 22) but not to 5 alpha-dihydrotestosterone, dehydroepiandrosterone, or androstenedione levels. We conclude that our novel bioassay enables quantitation of mammalian cell response to bioactive androgens in human serum, even in pediatric patients with relatively low androgen levels.
我们开发了一种哺乳动物细胞(COS-1)生物测定法,该方法能够直接从少量(10微升)人血清中测量雄激素生物活性。该重组测定法基于雄激素受体(AR)的配体结合域与N端区域之间的雄激素依赖性相互作用,它们分别与酿酒酵母的Gal4 DNA结合域和单纯疱疹病毒VP16蛋白的转录激活域融合。细胞中AR相互作用蛋白3的共表达可放大这种相互作用。报告质粒在荧光素酶基因上游含有5个Gal4结合位点;细胞裂解物中的荧光素酶活性源自人血清中的雄激素生物活性。胎牛血清中睾酮的饱和浓度可使相对荧光素酶活性诱导增加700倍以上。胎牛血清中该测定法对睾酮的灵敏度小于1.0纳摩尔/升。测定法的批内和批间变异系数分别为8.3%和21%。非甾体类抗雄激素可阻断AR末端之间的相互作用,并且该测定法与17β-雌二醇的交叉反应最小。我们对23名青春期体质性延迟的男孩(13.9 - 16.8岁)和9名青春期前隐睾症男孩(1.0 - 6.4岁)的血清雄激素生物活性进行了研究。在15名青春期体质性延迟的男孩以及所有接受人绒毛膜促性腺激素治疗(范围为1.0 - 14.5纳摩尔/升睾酮当量)的隐睾症男孩中均可检测到雄激素生物活性。通过该生物测定法测得的血清雄激素生物活性与血清睾酮浓度密切相关(r = 0.93,P < 0.0001,n = 22),但与5α-双氢睾酮、脱氢表雄酮或雄烯二酮水平无关。我们得出结论,我们的新型生物测定法能够定量人血清中生物活性雄激素引起的哺乳动物细胞反应,即使是雄激素水平相对较低的儿科患者也适用。