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作 者:李昕[1,2] 谢胜男[1,2] 殷娟娟[1,2] 刘光伟[1,2] 李尧华[1,2] 吕国蔚[3] 于顺[1,2,3]
机构地区:[1]首都医科大学宣武医院老年病研究所神经生物学研究室,北京100053 [2]首都医科大学宣武医院教育部神经变性病学重点实验室,北京100053 [3]首都医科大学宣武医院低氧医学研究所,北京100053
出 处:《基础医学与临床》2009年第12期1254-1257,共4页Basic and Clinical Medicine
基 金:国家自然科学基金(30270482;30271437;30570646;30430280);北京市自然科学基金(7022011)
摘 要:目的探讨小鼠在重复急性低氧暴露后脑组织中的糖酵解、线粒体氧化磷酸化及能量负荷的变化。方法成年BALB/c小鼠重复低氧暴露5次,测定每次低氧暴露时的平均耐受时间、体温及第0、1、3、5次低氧暴露后脑组织中的磷酸果糖激酶(PFK)、丙酮酸激酶(PK)、线粒体复合体Ⅰ活性和磷酸腺苷水平。结果重复低氧暴露使小鼠低氧耐受性增强,体温降低,脑组织中PFK和PK活性先增高后降低,复合体Ⅰ活性持续降低,能量负荷保持稳定。结论重复急性低氧使小鼠脑组织的糖酵解活性出现规律性变化,线粒体的氧化磷酸化受抑制,但能量负荷保持稳定。Objective To study the effects of repeated hypoxic exposures(HEs) on glycolysis,mitochondrial oxidative phosphorylation and energy charge in mouse brain.Methods Adult BALB/c mice were repeatedly exposed to hypoxia for 5 times and the standard tolerant time and body temperature were recorded.The activities of PFK,PK and mitochondrial complex I in the brain were assayed.Phosphoadenosines and energy charge were measured.Results Repeated HEs prolonged the hypoxic tolerance and reduced the body temperature.The activities of PFK and PK experienced regular changes,with an increase in 1st and 3rd HEs and a decline to control levels in 5th HE.The complex I activity continued to decrease during HEs.The energy charge was stable.ConclusionHEs lead to a regular change of glycolysis,a continued inhibition of mitochondrial oxidative phosphorylation,and a maintained energy charge in the brains of mouse.
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