Histologic, immunocytologic and subcellular changes in the rat adenohypophysis caused by prolactin, growth hormone and ACTH-producing transplanted pituitary tumors: A comparison with spontaneous prolactin-producing adenomas

D.J. McComb , G. Ilse , N. Ryan , E. Horvath , K. Kovacs , E. Nagy , I. Berczi
{"title":"Histologic, immunocytologic and subcellular changes in the rat adenohypophysis caused by prolactin, growth hormone and ACTH-producing transplanted pituitary tumors: A comparison with spontaneous prolactin-producing adenomas","authors":"D.J. McComb ,&nbsp;G. Ilse ,&nbsp;N. Ryan ,&nbsp;E. Horvath ,&nbsp;K. Kovacs ,&nbsp;E. Nagy ,&nbsp;I. Berczi","doi":"10.1016/S0014-4908(80)80051-2","DOIUrl":null,"url":null,"abstract":"<div><p>The effects of three transplanted pituitary adenomas on the intrasellar nontumorous adenohypophysis of rats hosting these tumors were investigated by histology, immunocytochemistry and electron microscopy. The first two tumors, designated MtT. W5 and MtT. W10 secreted prolactin and growth hormone, while the third, MtT. F4 produced prolactin and ACTH.</p><p>The intrasellar pituitaries appeared smaller, immunocytochemistry demonstrated a reduction in prolactin positivity in the anterior pituitaries of rats hosting MtT. W10 and MtT. F4 tumors. A similar reduction was noted for growth hormone in the adenohypophysis of rats bearing MtT. W5 and MtT. W10 tumor implants. Ultrastructural investigation revealed an apparent decrease in secretory granule size associated with a reduction in cell volume in the mammotrophs, somatotrophs and corticotrophs exposed to hypersecretion of their respective hormones. The number of cytoplasmic organelles appeared to be diminished. It was apparent that in rats with transplanted pituitary tumors, a feedback mechanism exists, altering the morphology of the respective nontumorous adenohypophysial cells and presumably inhibiting their secretory activity.</p><p>These changes were compared with a prolactin-secreting adenoma arising spontaneously in the pituitaries of aging Long-Evans rats. In these animals, the pituitaries were enlarged and the number of immunoreactive mammotrophs in the nontumorous portions of the adenohypophysis was markedly increased. The fine structural morphology of the nontumorous mammotrophs differed from those in the previous three groups, and was consistent with increased secretory activity similar to that found in normal lactating rats. These findings support the assumption that the morphologic features of these mammotrophs were not affected by prolactin secretion of the tumor.</p></div>","PeriodicalId":75841,"journal":{"name":"Experimentelle Pathologie","volume":"18 4","pages":"Pages 213-222"},"PeriodicalIF":0.0000,"publicationDate":"1980-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0014-4908(80)80051-2","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimentelle Pathologie","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0014490880800512","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 9

Abstract

The effects of three transplanted pituitary adenomas on the intrasellar nontumorous adenohypophysis of rats hosting these tumors were investigated by histology, immunocytochemistry and electron microscopy. The first two tumors, designated MtT. W5 and MtT. W10 secreted prolactin and growth hormone, while the third, MtT. F4 produced prolactin and ACTH.

The intrasellar pituitaries appeared smaller, immunocytochemistry demonstrated a reduction in prolactin positivity in the anterior pituitaries of rats hosting MtT. W10 and MtT. F4 tumors. A similar reduction was noted for growth hormone in the adenohypophysis of rats bearing MtT. W5 and MtT. W10 tumor implants. Ultrastructural investigation revealed an apparent decrease in secretory granule size associated with a reduction in cell volume in the mammotrophs, somatotrophs and corticotrophs exposed to hypersecretion of their respective hormones. The number of cytoplasmic organelles appeared to be diminished. It was apparent that in rats with transplanted pituitary tumors, a feedback mechanism exists, altering the morphology of the respective nontumorous adenohypophysial cells and presumably inhibiting their secretory activity.

These changes were compared with a prolactin-secreting adenoma arising spontaneously in the pituitaries of aging Long-Evans rats. In these animals, the pituitaries were enlarged and the number of immunoreactive mammotrophs in the nontumorous portions of the adenohypophysis was markedly increased. The fine structural morphology of the nontumorous mammotrophs differed from those in the previous three groups, and was consistent with increased secretory activity similar to that found in normal lactating rats. These findings support the assumption that the morphologic features of these mammotrophs were not affected by prolactin secretion of the tumor.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
泌乳素、生长激素和促acth移植垂体瘤引起大鼠垂体的组织学、免疫细胞学和亚细胞改变:与自发性催乳素腺瘤的比较
采用组织学、免疫细胞化学和电镜观察3种垂体腺瘤移植对荷瘤大鼠鞍内非瘤性腺垂体的影响。前两个肿瘤,命名为MtT。W5和MtT。W10分泌催乳素和生长激素,MtT分泌催乳素和生长激素。F4产生催乳素和促肾上腺皮质激素。鞍内垂体变小,免疫细胞化学显示MtT大鼠垂体前叶催乳素阳性降低。W10和MtT。F4肿瘤。在携带MtT的大鼠腺垂体中,生长激素也出现了类似的减少。W5和MtT。W10肿瘤植入物。超微结构研究显示,乳腺营养细胞、生长营养细胞和皮质营养细胞在各自激素分泌旺盛的情况下,分泌颗粒大小明显减少,细胞体积减少。胞质细胞器数量减少。很明显,在移植垂体瘤的大鼠中,存在一种反馈机制,改变了相应的非肿瘤腺垂体细胞的形态,并可能抑制了它们的分泌活性。这些变化与衰老的龙-埃文斯大鼠垂体中自发产生的催乳素分泌腺瘤进行了比较。在这些动物中,垂体肿大,腺垂体非肿瘤部分的免疫反应性乳腺肥大细胞数量明显增加。非肿瘤乳腺营养细胞的精细结构形态与前三组不同,并且与正常哺乳期大鼠相似的分泌活性增加一致。这些发现支持了乳腺肥大细胞的形态特征不受肿瘤泌乳素分泌影响的假设。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Author Index Subject Index Errata Editorial Board A contribution to the postnatal enzymatic state of maturity of gyrus hippocampi in the embryofetal alcohol syndrome of the rat
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1