Grootenhuis A J, van Sluijs F J, Klaij I A, Steenbergen J, Timmerman M A, Bevers M M, Dieleman S J, de Jong F H
Department of Biochemistry (Division of Chemical Endocrinology), Erasmus University Rotterdam, The Netherlands.
J Endocrinol. 1990 Nov;127(2):235-42. doi: 10.1677/joe.0.1270235.
Inhibin bioactivity and mRNA for inhibin subunits were measured in four dog Sertoli cell tumours and in the testes of five normal control dogs. The tumours contained increased levels of inhibin (P less than 0.05) and mRNA for the alpha and beta B subunits when compared with controls, whereas the mRNA for the beta A subunit was not detected in tumours or control testes. The inhibin bioactivity was associated with a 32 kDa molecule in both Sertoli cell tumours and normal dog testes; no higher molecular weight forms were found after sodium dodecyl sulphate-polyacrylamide gel electrophoresis. Peripheral levels of immunoassayable inhibin in dogs with Sertoli cell tumours were higher than those in the controls (P = 0.01), indicating that it might be possible to use this parameter as a marker for Sertoli cell tumours. Other testicular tumours, however, might also secrete immunoactive inhibin. The increased inhibin concentrations are likely to be the cause of the suppressed peripheral levels of FSH (P less than 0.02). However, peripheral levels of LH (P less than 0.02) and testosterone (P less than 0.01) were also suppressed in the dogs with Sertoli cell tumours, whereas the concentrations of oestradiol in the peripheral plasma of both groups did not differ. Finally, i.v. injection of the LHRH agonist buserelin caused a significant increase in LH and testosterone in the control dogs, but not in the dogs with Sertoli cell tumours. It was concluded that secretory products from the Sertoli cell tumours suppressed pituitary gonadotrophin secretion. It is unlikely that testosterone or oestradiol play a role in this respect. FSH may be suppressed by the high levels of inhibin in tumour-bearing dogs, but it remains unclear whether inhibin or another Sertoli cell product is responsible for the unresponsiveness of the pituitary gland to LHRH and the suppression of LH.
在四个犬睾丸支持细胞瘤以及五只正常对照犬的睾丸中检测了抑制素生物活性和抑制素亚基的mRNA。与对照组相比，肿瘤中抑制素水平升高（P<0.05），α和βB亚基的mRNA水平也升高，而在肿瘤或对照睾丸中未检测到βA亚基的mRNA。在支持细胞瘤和正常犬睾丸中，抑制素生物活性均与一个32 kDa的分子相关；十二烷基硫酸钠-聚丙烯酰胺凝胶电泳后未发现更高分子量的形式。患有支持细胞瘤的犬外周血中可免疫检测的抑制素水平高于对照组（P = 0.01），表明该参数可能可作为支持细胞瘤的标志物。然而，其他睾丸肿瘤也可能分泌免疫活性抑制素。抑制素浓度升高可能是外周血FSH水平降低的原因（P<0.02）。然而，患有支持细胞瘤的犬外周血LH水平（P<0.02）和睾酮水平（P<0.01）也降低，而两组外周血浆中雌二醇浓度无差异。最后，静脉注射促性腺激素释放激素激动剂布舍瑞林可使对照犬的LH和睾酮显著升高，但对患有支持细胞瘤的犬无效。得出的结论是，支持细胞瘤的分泌产物抑制了垂体促性腺激素的分泌。在这方面，睾酮或雌二醇不太可能起作用。FSH可能被患肿瘤犬体内高水平的抑制素所抑制，但尚不清楚是抑制素还是其他支持细胞产物导致垂体对LHRH无反应以及LH被抑制。
