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Elevated levels of mitochonrial respiratory complexes activities and ATP production in 17-β-estradiol-induced prolactin-secretory tumor cells in male rats are inhibited by melatonin in vivo and in vitro

摘要Background Our earlier studies indicate that melatonin inhibits the proliferation of prolactinoma and induces apoptosis of pituitary prolactin-secreting tumor in rats.Melatonin has also been shown to induce apoptosis and to reduce the production of ATP in breast tumor cells.This study analyzed the levels of the four mitochondrial respiratory complexes and the production of ATP and also the effects of melatonin treatment of prolactinoma.Methods In the in vivo study,mitochondria were harvested from control pituitaries or prolactinoma collected from the pituitaries of melatonin-and 17-β-estradiol (E2)-treated male rats.In the in vitro study,prolactinoma cells mitochondria were harvested.Activities of the four mitochondrial respiratory complexes were assayed using fluorometer.ATP production of prolactinoma cells was estimated using bioluminescent methods.Results Elevated levels of four mitochondrial respiratory complexes activities and ATP production were recorded in prolactinoma cells.Moreover,in both in vivo and in vitro studies,melatonin inhibited the activities of mitochondrial respiratory complexes and the production of ATP in prolactinoma cells.Conclusions There is a link between mitochondrial function increase and tumorigenesis.Melatonin induces apoptosis of pituitary prolactin-secreting tumor of rats via the induction of mitochondrial dysfunction and inhibition of energy metabolism.

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作者单位 Department of General Surgery, Shijingshan Teaching Hospital of Capital Medical University, Beijing Shijingshan Hospital, Beijing 100043, China [1] Department of Critical Care Medicine, Cancer Hospital and Institute,Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China [2] Department of Physiology, Institute of Basic Medical Sciences,Chinese Academy of Medical Sciences, School of Basic Medicine,Peking Union Medical College, Beijing 100005, China [3] Department of Toxicology, National Institute of Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China [4]
栏目名称 ORIGINAL ARTICLES
DOI 10.3760/cma.j.issn.0366-6999.20131965
发布时间 2014-01-18
基金项目
This study was supported by grants from the National Natural Science Foundation of China Beijing Natural Science Foundation of China Fund of the National Ministry of Science and Technology of China (No.2003ccc01300) to XU Rong-kun,and China Postdoctoral Science Foundation to YANG Quan-hui
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中华医学杂志(英文版)

中华医学杂志(英文版)

2013年126卷24期

4724-4730页

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