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急性重复低氧对小鼠脑组织中糖酵解和线粒体氧化磷酸化以及能量负荷的影响
引用本文:李昕,谢胜男,殷娟娟,刘光伟,李尧华,吕国蔚,于顺. 急性重复低氧对小鼠脑组织中糖酵解和线粒体氧化磷酸化以及能量负荷的影响[J]. 基础医学与临床, 2009, 29(12): 1254-1257
作者姓名:李昕  谢胜男  殷娟娟  刘光伟  李尧华  吕国蔚  于顺
作者单位: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;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;首都医科大学,宣武医院,低氧医学研究所,北京100053;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;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;首都医科大学,宣武医院,低氧医学研究所,北京100053
基金项目:国家自然科学基金,北京市自然科学基金
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。

关 键 词:低氧  磷酸果糖激酶  丙酮酸激酶  线粒体复合体Ⅰ  能量负荷
收稿时间:2009-02-24
修稿时间:2009-05-06

Effects of repeated hypoxic exposures on glycolysis, mitochondrial oxidative phosphorylation and energy charge in mouse brain
LI Xin,XIE Sheng-nan,YIN Juan-juan,LIU Guang-wei,LI Yao-hua,L Guo-wei,YU Shun. Effects of repeated hypoxic exposures on glycolysis, mitochondrial oxidative phosphorylation and energy charge in mouse brain[J]. Basic Medical Sciences and Clinics, 2009, 29(12): 1254-1257
Authors:LI Xin  XIE Sheng-nan  YIN Juan-juan  LIU Guang-wei  LI Yao-hua  L Guo-wei  YU Shun
Affiliation:LI Xin,XIE Sheng-nan,YIN Juan-juan,LIU Guang-wei,LI Yao-hua,L(U) Guo-wei,YU Shun
Abstract:Objective To study the effects of repeated hypoxic exposures (HEs) on glycolysis, mitochondrial oxi-dative 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. Conclusion HEs lead to a regular change of glycolysis, a continued inhibition of mitochondrial oxidative phosphorylation, and a main-tained energy charge in the brains of mouse.
Keywords:hypoxia  phosphofructokinase  pyruvate kinase  mitochondrial complex Ⅰ  energy charge
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