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首页> 外文期刊>Journal of Cellular Physiology >Nandrolone and stanozolol induce leydig cell tumor proliferation through an estrogen-dependent mechanism involving IGF-I system
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Nandrolone and stanozolol induce leydig cell tumor proliferation through an estrogen-dependent mechanism involving IGF-I system

机译：诺龙和康力龙诱导睾丸间质细胞瘤通过一个estrogen-dependent扩散机制涉及IGF-I系统

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Several substances such as anabolic androgenic steroids (AAS), peptide hormones like insulin-like growth factor-I (IGF-I), aromatase inhibitors and estrogen antagonists are offered via the Internet, and are assumed without considering the potential deleterious effects that can be caused by their administration. In this study we aimed to determine if nandrolone and stanozolol, two commonly used AAS, could have an effect on Leydig cell tumor proliferation and if their effects could be potentiated by the concomitant use of IGF-I. Using a rat Leydig tumor cell line, R2C cells, as experimental model we found that nandrolone and stanozolol caused a dose-dependent induction of aromatase expression and estradiol (E2) production. When used in combination with IGF-I they were more effective than single molecules in inducing aromatase expression. AAS exhibited estrogenic activity and induced rapid estrogen receptor (ER)-dependent pathways involving IGF1R, AKT, and ERK1/2 phosphorylation. Inhibitors for these kinases decreased AAS-dependent aromatase expression. Up-regulated aromatase levels and related E2 production increased cell proliferation as a consequence of increased cyclin E expression. The observation that ER antagonist ICI182,780 was also able to significantly reduce ASS- and AAS+IGF-induced cell proliferation, confirmed a role for estrogens in AAS-dependent proliferative effects. Taken together these data clearly indicate that the use of high doses of AAS, as it occurs in doping practice, enhances Leydig cell proliferation, increasing the risk of tumor development. This risk is higher when AAS are used in association with IGF-I. To our knowledge this is the first report directly associating AAS and testicular cancer.
机译：等物质合成雄激素的类固醇(AAS)、肽激素胰岛素样生长因子(IGF-I),芳香化酶抑制剂和雌激素拮抗剂通过互联网,认为没有考虑到潜在的有害的影响可能是由于他们的政府。本研究旨在确定诺龙康力龙、两个常用的原子吸收光谱法,可以对睾丸间质细胞瘤增殖和产生影响如果他们可能会影响伴随IGF-I的使用。肿瘤细胞系,R2C细胞实验模型我们发现诺龙和康力龙造成芳香化酶表达的诱导存在剂量依赖的相关性和雌二醇(E2)的生产。结合IGF-I他们更有效比单分子诱导芳香化酶表达式。诱导快速雌激素受体(ER)端依赖涉及IGF1R的途径,一种蛋白激酶,ERK1/2磷酸化。减少AAS-dependent芳香化酶表达。差异芳香化酶E2水平和相关生产增加细胞增殖细胞周期素E表达增加的结果。观察ER拮抗剂ICI182,780也能显著降低的屁股,原子吸收光谱法+ IGF-induced细胞增殖,证实了角色AAS-dependent增生性的雌激素效果。表明高剂量的原子吸收光谱法的使用,因为它发生在掺杂实践,提高睾丸间质细胞扩散,增加肿瘤的风险发展。用于与IGF-I协会。这是第一个报告直接将原子吸收光谱法和睾丸癌。

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