Effects of cysteamine on pituitary, MTTW15 tumor, and serum prolactin levels measured by rat lymphoma cell bioassay and radioimmunoassay.
Effects of cysteamine on pituitary, MTTW15 tumor, and serum prolactin levels measured by rat lymphoma cell bioassay and radioimmunoassay.
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通过大鼠淋巴瘤细胞生物测定和放射免疫测定测定半胱胺对垂体、MTTW15 肿瘤和血清催乳素水平的影响。
DOI：
10.1210/endo-114-5-1812
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发表时间：
1984
期刊：
影响因子：
4.8
通讯作者：
M. A. Hartfel
中科院分区：
文献类型：
--
作者：
J. Parsons;E. K. Peterson;M. A. Hartfel
半胱胺 (CSH) 是一种巯基化合物，可降低放射免疫分析 (RIA) 测定的血清和垂体前叶 (AP) 泌乳素 (PRL)。我们使用 PRL 的 Nb2 淋巴瘤细胞生物测定 (BIO) 来评估雄性和 MtTW15 荷瘤雌性大鼠血清和组织中 PRL 水平可能与 CSH 相关的变化。实验动物单次皮下注射CSH（300 mg/kg），0.5-24小时后采集样本。由于 CSH 和 CSH 大鼠血清在 BIO 中具有毒性，因此在测定前对样品进行透析。所有样品均通过 RIA 评估 PRL 和 GH。 CSH后0.5小时，雄性大鼠BIO血清PRL明显下降（P小于0.05）； 24小时内水平保持在较低水平。 RIA 测定的血清 PRL 在 4 小时时显着降低，但在 0.5 小时或 24 小时时没有显着降低。 BIO 和 RIA 始终降低 AP 提取物中的 PRL (60-90%)。 4小时后，肿瘤大鼠的血清和组织（AP和肿瘤）中记录到BIO和RIA可检测到的PRL显着降低。连续放血（0.5-4小时）的CSH治疗荷瘤大鼠显示，通过BIO和RIA，1小时和4小时血清PRL分别降低50%和80%。 CSH 对任何时间间隔研究的任何动物的血清和组织中的 GH 水平没有影响。我们的结果证实了早期关于 CSH 引起 RIA 可检测 PRL 降低的报道。他们表明，这种变化不能仅归因于检测效果，因为 BIO 可以明显看出循环和储存的 PRL（AP 和肿瘤）显着下降。组织提取物的结果最为引人注目。他们建议 CSH 或具有储存 PRL 的代谢中间体的作用，可减少可提取的 PRL 和激素释放。其他人已经提出了 CSH 对 PRL 提取的这种影响。无论机制如何，它似乎都相对具体，因为 GH 细胞没有受到影响。
Cysteamine (CSH), a sulfhydryl compound, reduces both serum and anterior pituitary (AP) PRL measured by RIA. We have used the Nb2 lymphoma cell bioassay (BIO) for PRL to evaluate possible CSH-related changes in PRL levels in sera and tissues of male and MtTW15 mammosomatotropic tumor-bearing female rats. Experimental animals received a single sc injection of CSH (300 mg/kg), and samples were collected 0.5-24 h later. Since CSH and serum from CSH rats were toxic in BIO, samples were dialyzed before assay. All samples were evaluated for PRL and GH by RIA as well. A significant decrease (P less than 0.05) in BIO serum PRL was evident in male rats 0.5 h after CSH; levels remained low for 24 h. Serum PRL by RIA was significantly depressed at 4 h but not at 0.5 h or 24 h. PRL in AP extracts was decreased (60-90%) at all times by BIO and RIA. Significant decreases of BIO- and RIA-detectable PRL were recorded in serum and tissues (AP and tumors) at 4 h in tumor rats. Sequentially bled (0.5-4 h) CSH-treated tumor-bearing rats showed 50% and 80% reductions in serum PRL at 1 and 4 h by both BIO and RIA. CSH had no effect on GH levels in sera and tissues of any animal studied at any time interval. Our results substantiate earlier reports on CSH-induced decreases in RIA-detectable PRL. They show that such changes cannot be attributed to assay effects alone, as significant decreases in circulating and stored PRL (both AP and tumor) were evident by BIO. Results with tissue extracts were the most dramatic. They suggest an action of CSH or a metabolic intermediate with stored PRL which reduces both extractable PRL and hormone release. Such an effect of CSH on PRL extraction has been suggested by others. Whatever the mechanism, it appears to be relatively specific, since GH cells were not affected.