Antioxidant mechanisms in apolipoprotein E deficient mice prior to and following closed head injury
Antioxidant mechanisms in apolipoprotein E deficient mice prior to and following closed head injury
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DOI：
10.1016/s0925-4439(99)00010-1
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发表时间：
1999-03-30
影响因子：
6.2
通讯作者：
Michaelson, DM
中科院分区：
文献类型：
--
作者：
Lomnitski, L;Chapman, S;Michaelson, DM
载脂蛋白E缺陷小鼠具有明显的记忆缺陷和神经化学紊乱，并且它们从闭合性头部损伤中的恢复受损。在本研究中，我们研究了载脂蛋白E缺陷小鼠的神经元紊乱与氧化应激相关的可能性，这反过来又影响了它们从闭合性头部损伤中恢复的能力。结果发现，载脂蛋白E缺陷小鼠的脑磷脂水平低于对照组（对照组的55 ± 15%，P < 0.01），两组小鼠的胆固醇水平相似，载脂蛋白E缺陷小鼠的共轭二烯水平高于对照组（132 ± 15%，P < 0.01）。载脂蛋白E缺陷小鼠脑内锰超氧化物歧化酶（134 +/- 7%），过氧化氢酶（122 +/- 8%）和谷胱甘肽还原酶（167 +/- 7%）活动高于对照组（P < 0.01），而谷胱甘肽过氧化物酶活性以及还原型谷胱甘肽和抗坏血酸水平在两个小鼠组中相似，闭合性头部损伤增加过氧化氢酶和谷胱甘肽过氧化物酶的活性在两个小鼠组，而谷胱甘肽还原酶增加，只有在对照组小鼠。两组超氧化物歧化酶活性均不受影响。这些研究结果表明，载脂蛋白E缺陷小鼠的抗氧化代谢改变之前和之后的头部损伤和抗氧化机制可能发挥作用，介导的神经元的维护和修复紊乱的载脂蛋白E缺陷小鼠。(C)1999 Elsevier Science B. V.保留所有权利。
Apolipoprotein E deficient mice have distinct memory deficits and neurochemical derangements and their recovery from closed head injury is impaired. In the present study, we examined the possibility that the neuronal derangements of apolipoprotein E deficient mice are associated with oxidative stress, which in turn affects their ability to recover from close head injury. It was found that brain phospholipid levels in apolipoprotein E deficient mice are lower than those of the controls (55 +/- 15% of control, P < 0.01), that the cholesterol levels of the two mice groups are similar and that the levels of conjugated dienes of the apolipoprotein E deficient mice are higher than those of control mice (132 +/- 15% of P < 0.01). Brains of apolipoprotein E deficient mice had higher Mn-superoxide dismutase (134 +/- 7%), catalase (122 +/- 8%) and glutathione reductase (167 +/- 7%) activities than control (P < 0.01), whereas glutathione peroxidase activity and the levels of reduced glutathione and ascorbic acid were similar in the two mouse groups, Closed head injury increased catalase and glutathione peroxidase activities in both mouse groups, whereas glutathione reductase increased only in control mice. The superoxide dismutase activity was unaffected in both groups. These findings suggest that the antioxidative metabolism of apolipoprotein E deficient mice is altered both prior to and following head injury and that antioxidative mechanisms may play a role in mediating the neuronal maintenance and repair derangements of the apolipoprotein E deficient mice. (C) 1999 Elsevier Science B.V. All rights reserved.