Department of Dental Technology and Materials Science, Central Taiwan University of Science and Technology, No.666, Buzih Road, Beitun District, Taichung 406, Taiwan.
Biol Trace Elem Res. 2013 Apr;152(1):66-74. doi: 10.1007/s12011-012-9596-1. Epub 2013 Jan 19.
Proper trace element level and antioxidant enzyme activity are crucial for the brain in maintaining normal neurological functions. To our knowledge, alteration of lipid peroxidation status, trace element level, and antioxidant activity in the homogenates of brain cortex after cerebral ischemia in gerbil, however, has not been investigated so far. Male Mongolian gerbils were divided into control and ischemic subjects. Cerebral ischemia was induced by occlusion of the right middle cerebral artery and right common carotid artery for 1 h. Experimental results showed that a significant increase (P < 0.01) of the malondialdehyde level was found in the ischemic brain as compared with the control group. Trace element analysis indicated that a remarkable elevation (P < 0.01) of the level of iron (Fe), chromium (Cr), and a statistical decrease of selenium (Se) and zinc (Zn) (P < 0.05) concentration were observed in the ischemic brain as compared with the control subject. No significant change (P > 0.05) of the copper (Cu) level was found in both experimental groups. Additionally, antioxidant activity of superoxide dismutase (P < 0.01) and catalase (P < 0.05) was significantly decreased in the ischemic brain as compared with the control subject. Taking all results together, it is conceivable to manifest the experimental findings that cerebral ischemia not only may result in an enhanced oxidative stress but also may lead to further oxidative injury. Moreover, disturbance of trace element level combined with declined antioxidant activity seems to play a significant role in responsible for the etiology of cerebral ischemia.
适当的微量元素水平和抗氧化酶活性对大脑维持正常神经功能至关重要。据我们所知,迄今为止,还没有研究过沙鼠大脑皮质缺血后脂质过氧化状态、微量元素水平和抗氧化活性的变化。雄性蒙古沙鼠分为对照组和缺血组。通过阻断右侧大脑中动脉和右侧颈总动脉 1 小时来诱导脑缺血。实验结果表明,与对照组相比,缺血大脑中的丙二醛水平显著升高(P<0.01)。微量元素分析表明,与对照组相比,缺血大脑中的铁(Fe)、铬(Cr)水平显著升高(P<0.01),硒(Se)和锌(Zn)浓度统计学上降低(P<0.05)。实验组铜(Cu)水平无明显变化(P>0.05)。此外,与对照组相比,缺血大脑中超氧化物歧化酶(P<0.01)和过氧化氢酶(P<0.05)的抗氧化活性显著降低。综合所有结果可以看出,实验结果表明,脑缺血不仅可能导致氧化应激增强,还可能导致进一步的氧化损伤。此外,微量元素水平的紊乱和抗氧化活性的下降似乎在脑缺血的病因中起着重要作用。