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机构地区:[1]湖南科技大学体育学院,中国湖南湘潭410200 [2]湖南城市学院体育系,中国湖南益阳410300 [3]湖南师范大学生命科学学院,中国湖南长沙410081
出 处:《生命科学研究》2011年第4期283-289,共7页Life Science Research
基 金:国家自然科学基金资助项目(30971413);湖南科技大学博士启动基金资助项目(E51090)
摘 要:脂质过氧化中间产物丙二醛(Malondialdehyde,MDA)在生物体内表现了广泛的生物毒性,MDA也是机体过度训练和运动性疲劳的重要生理指标.采用光学显微镜和透射式电子显微镜观察不同浓度MDA作用后海马神经元形态和超微结构的变化,并采用荧光分光光度法测定原代培养的海马神经元中Ca2+-ATPase活性的变化和胞质游离钙离子水平的变化,探讨MDA对海马神经元形态和结构上的破坏及神经元钙离子稳态的影响.在光镜下可观察到MDA作用下神经元突触变短,胞体肿胀,出现细胞死亡或凋亡的形态特征;在电镜下可观察到线粒体结构的明显破坏,内膜上的嵴颗粒减少或消失;同时MDA还通过抑制质膜Ca2+-ATPase的活性和其它的途径,破坏神经元胞质游离Ca2+稳态.结果表明,MDA可通过破坏海马神经元的结构和影响胞质中钙离子稳态,破坏神经元的生理功能,在机体运动性中枢疲劳形成中可能发挥重要作用.As a useful physiological index for over trained or exercise-induced fatigue, there were kinds of biological toxicity of malondialdehyde (MDA) produced in the process of lipid peroxidation. In this investigation, in order to observe the effects of MDA on the damages of hippocampal neuronal shapes and ultra-structure, and examine the calcium homeostasis in primary culture neurons, the microscope and transmission electronic microscope were applied for observing the changes of shapes and the transforms of ultra-structures, and also, the fluorospectrophotometer was used to determine the concentration of cytosolic free calcium in the system of primary culture hippocampal neurons of SD rats. The mierophotographic study clearly demonstrated that the hippocampal neurons became gradually damaged following exposure to different concentrations of MDA. And also, the ultra-structures were observed that the architectures of mitochondria were deformed and their cristae were decreased or disappeared with the increasing of MDA concentration. Further study indicated that the plasma membrance Ca^2+-ATPase (PMCA) activity was inhibited by MDA in a concentration (1.0-1 000 μmol/L) and time (30 min) dependent manner, hence, induced to damage the calcium homeostasis in primary culture hippocampal neurons. It was hinted that MDA was one of the important elements induced to exercise-induced fatigue by damaging the structures of hippocampal neuron and disturbance of Ca^2+ homeostasis.
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