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醌蛋白加合物在老年大鼠的黑质中积累,并与 SH-SY5Y 细胞中多巴胺诱导的毒性相关。

Quinoprotein adducts accumulate in the substantia nigra of aged rats and correlate with dopamine-induced toxicity in SH-SY5Y cells.

机构信息

School of Life Science, East China Normal University, Zhongshan bei lu 3663, Shanghai 200062, China.

出版信息

Neurochem Res. 2011 Nov;36(11):2169-75. doi: 10.1007/s11064-011-0541-z. Epub 2011 Jul 22.

Abstract

Parkinson's disease (PD) is an age-dependent neurodegenerative disorder characterized by dopaminergic neuron loss in substantia nigra. Previous studies have implicated a role of dopamine oxidation in PD. Dopamine oxidation leads to the formation of dopamine quinone, which generates reactive oxygen species and covalently modifies cysteinyl proteins to form quinoprotein adduct. We compared quinoprotein adduct formation and lipid peroxidation in different brain regions of young and old rats. We found a prominent age-dependent accumulation of quinoprotein adducts in the substantia nigra, while no significant change of lipid peroxidation was detected in any brain regions of 2- to 15-month old rats. To determine whether quinoprotein adduct formation correlates with dopamine-induced cytotoxicity, we analyzed dopamine treated SH-SY5Y cells and found a strong correlation between quinoprotein adduct formation and cytotoxicity. Together, our results indicate that quinoprotein adduct formation may play a role in the age-dependent selective vulnerability of dopaminergic neurons in PD.

摘要

帕金森病(PD)是一种与年龄相关的神经退行性疾病,其特征是黑质中多巴胺能神经元的丧失。先前的研究表明,多巴胺氧化在 PD 中起作用。多巴胺氧化导致多巴胺醌的形成,后者会产生活性氧,并使半胱氨酸蛋白共价修饰形成醌蛋白加合物。我们比较了年轻和老年大鼠不同脑区的醌蛋白加合物形成和脂质过氧化。我们发现,醌蛋白加合物在黑质中的积累随年龄的增长而显著增加,而在 2 至 15 月龄大鼠的任何脑区均未检测到脂质过氧化的显著变化。为了确定醌蛋白加合物的形成是否与多巴胺诱导的细胞毒性相关,我们分析了多巴胺处理的 SH-SY5Y 细胞,发现醌蛋白加合物的形成与细胞毒性之间存在很强的相关性。总之,我们的结果表明,醌蛋白加合物的形成可能在 PD 中多巴胺能神经元的年龄依赖性选择性易损性中起作用。

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