Maser Edmund
Institute of Toxicology and Pharmacology for Natural Scientists, University Medical School Schleswig-Holstein, Campus Kiel, Brunswiker Str. 10, 24105 Kiel, Germany.
Biochem Biophys Res Commun. 2006 Feb 24;340(4):1019-22. doi: 10.1016/j.bbrc.2005.12.113. Epub 2005 Dec 28.
Oxidative stress is increasingly implicated in neurodegenerative disorders including Alzheimer's, Parkinson's, Huntington's, and Creutzfeld-Jakob diseases or amyotrophic lateral sclerosis. Reactive oxygen species seem to play a significant role in neuronal cell death in that they generate reactive aldehydes from membrane lipid peroxidation. Several neuronal diseases are associated with increased accumulation of abnormal protein adducts of reactive aldehydes, which mediate oxidative stress-linked pathological events, including cellular growth inhibition and apoptosis induction. Combining findings on neurodegeneration and oxidative stress in Drosophila with studies on the metabolic characteristics of the human enzyme carbonyl reductase (CR), it is clear now that CR has a potential physiological role for neuroprotection in humans. Several lines of evidence suggest that CR represents a significant pathway for the detoxification of reactive aldehydes derived from lipid peroxidation and that CR in humans is essential for neuronal cell survival and to confer protection against oxidative stress-induced brain degeneration.
氧化应激与包括阿尔茨海默病、帕金森病、亨廷顿病、克雅氏病或肌萎缩侧索硬化症在内的神经退行性疾病的关联日益密切。活性氧似乎在神经元细胞死亡中起重要作用，因为它们通过膜脂质过氧化产生反应性醛类。几种神经疾病与反应性醛类的异常蛋白质加合物的积累增加有关，这些加合物介导氧化应激相关的病理事件，包括细胞生长抑制和凋亡诱导。将果蝇神经退行性变和氧化应激的研究结果与人类羰基还原酶（CR）代谢特征的研究相结合，现在很清楚CR在人类神经保护中具有潜在的生理作用。多条证据表明，CR是脂质过氧化衍生的反应性醛类解毒的重要途径，并且人类中的CR对于神经元细胞存活以及抵御氧化应激诱导的脑退化至关重要。
