Omar R, Pappolla M
Department of Pathology, West Virginia University School of Medicine, Morgantown 26506.
Eur Arch Psychiatry Clin Neurosci. 1993;242(5):262-7. doi: 10.1007/BF02190384.
We studied heat shock protein (HSP) synthesis by cultured human neuroblastoma cells in response to either hyperthermia or high levels of superoxide anion (oxygen free radical). Both treatment modalities resulted in induced synthesis of the same major HSP species with an additive effect on the latter and on cell growth inhibition upon combined treatments. Exposure to superoxide anion in the presence of the free radical scavenging enzymes, superoxide dismutase and catalase improved cell survival and prevented HSP induction. These findings suggest a common mechanism by which various forms of injury, such as hyperthermia, cause HSP induction, that is, via oxidative stress or increased production of oxygen free radicals. Increased expression of some HSPs has been detected in association with the pathological lesions that characterize some neurodegenerative diseases such as the neurofibrillary tangles of Alzheimer's disease. This, in turn, suggests that chronic oxidative stress may play a role in the pathogenesis of these disorders.
我们研究了培养的人神经母细胞瘤细胞对热疗或高水平超氧阴离子（氧自由基）的反应中热休克蛋白（HSP）的合成情况。两种处理方式均导致相同主要HSP种类的诱导合成，联合处理时对后者以及细胞生长抑制具有累加效应。在存在自由基清除酶超氧化物歧化酶和过氧化氢酶的情况下暴露于超氧阴离子可提高细胞存活率并阻止HSP的诱导。这些发现提示了一种共同机制，即诸如热疗等各种形式的损伤通过该机制导致HSP诱导，也就是说，通过氧化应激或氧自由基产生增加。在与某些神经退行性疾病（如阿尔茨海默病的神经原纤维缠结）相关的病理病变中已检测到一些HSP的表达增加。这反过来表明慢性氧化应激可能在这些疾病的发病机制中起作用。
