Melatonin protects against copper-mediated free radical damage
Melatonin protects against copper-mediated free radical damage
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DOI：
10.1034/j.1600-079x.2002.01859.x
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发表时间：
2002-05-01
影响因子：
10.3
通讯作者：
Daya, S
中科院分区：
文献类型：
--
作者：
Parmar, P;Limson, J;Daya, S
铜是一种必需的微量元素，它是许多酶的组成部分。虽然维持生命需要微量的铜，但过量的铜是剧毒的。铜与各种神经退行性疾病有关，如威尔逊病和阿尔茨海默病。以往的研究表明，褪黑激素，松果体的主要分泌产物，结合氯化铜（Cu2+），这可能有影响，铜诱导的神经退行性疾病。在本研究中，在体外诱导铜介导的脂质过氧化反应。褪黑激素（5毫米）保护铜介导的脂质过氧化肝匀浆。电子显微镜照片在体内施用的Cu 2+和褪黑激素显示，褪黑激素提供一定的保护，以大鼠肝细胞中的铜的存在。电化学研究表明，褪黑激素，除了结合Cu2+可以提供保护，对铜介导的自由基损伤结合Cu1+。这些研究结果为褪黑激素的神经保护作用提供了进一步的证据。
Copper is essential trace element which forms an integral component of many enzymes. While trace amounts of copper are needed to sustain life, excess copper is extremely toxic. Copper has been implicated in various neurodegenerative disorders, such as Wilson's and Alzheimer's diseases. Previous studies showed that melatonin, the principle secretory product of the pineal gland, binds Cupric chloride (Cu2+) and that this may have implications ill copper-induced neurodegenerative diseases. In the present Study, in vitro copper-mediated lipid peroxidation was induced. Melatonin (5 mM) protected against copper-mediated lipid peroxidation in liver homogenates. Electron micrographs of in vivo administered Cu2+ and melatonin show that melatonin affords some protection to rat hepatocytes in the presence of copper. Electrochemical studies performed show that melatonin, in addition to binding Cu2+ may provide protection against copper-mediated free radical damage by binding Cu1+. The findings of these studies provide further evidence for the neuroprotective role of melatonin.