机构地区:[1]Department of General Surgery, Shijingshan Teaching Hospital ofCapital Medical University, Beijing Shijingshan Hospital, Beijing100043, China [2]Department of Critical Care Medicine, Cancer Hospital and Institute,Chinese Academy of Medical Sciences and Peking Union MedicalCollege, Beijing 100021, China [3]Department of Physiology, Institute Of Basic Medical Sciences,Chinese Academy of Medical Sciences, School of Basic Medicine,Peking Union Medical College, Beijing 100005, China [4]Department of Toxicology, Nati-onal Institute of 0ccupaiionalHealth and Poison Control, Chinese Center for Disease Control andPrevention, Beijing 100050, China
出 处:《Chinese Medical Journal》2013年第24期4724-4730,共7页中华医学杂志(英文版)
基 金:Science Foundation of China (No. 30270507 and No. 30371581), Beijing Natural Science Foundation of China (No. 7022025), 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.
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 17-13-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 mitochondria[ 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.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 17-13-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 mitochondria[ 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.
关 键 词:apoptosis mitochondrial function PROLACTINOMA MELATONIN
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