Lipids status and copper in a single astrocyte of the rat model for amyotrophic lateral sclerosis: Correlative synchrotron-based X-ray and infrared imaging.,Journal of Biophotonics

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Lipids status and copper in a single astrocyte of the rat model for amyotrophic lateral sclerosis: Correlative synchrotron-based X-ray and infrared imaging.
Journal of Biophotonics ( IF 2.0 ) Pub Date : 2020-05-28 , DOI: 10.1002/jbio.202000069
Martin Kreuzer ₁ , Stefan Stamenković ₂ , Si Chen ₃ , Pavle Andjus ₂ , Tanja Dučić ₁

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease, causing death of motor neurons controlling voluntary muscles. The pathological mechanisms of the disease are only partially understood. The hSOD1‐G93A ALS rat model is characterized by an overexpression of human mutated SOD1, causing increased vulnerability by forming intracellular protein aggregates, inducing excitotoxicity, affecting oxidative balance and disturbing axonal transport. In this study we followed the bio‐macromolecular organic composition and compartmentalization together with trace metal distribution in situ in single astrocytes from the ALS rat model and compared them to the control astrocytes from nontransgenic littermates by simultaneous use of two synchrotron radiation‐based methods: Fourier transform infrared microspectroscopy (SR‐FTIR) and hard X‐ray fluorescence microscopy (XRF). We show that ALS cells contained more Cu, which colocalized with total lipids, increased carbonyl groups and oxidized lipids, thus implying direct involvement of Cu in oxidative stress of lipidic components without direct connection to protein aggregation in situ.

中文翻译：

肌萎缩性侧索硬化大鼠模型的单个星形胶质细胞中的脂质状态和铜：基于同步加速器的相关X射线和红外成像。

肌萎缩性侧索硬化症（ALS）是一种致命的神经退行性疾病，导致控制自愿肌肉的运动神经元死亡。该疾病的病理机制仅被部分理解。hSOD1-G93A ALS大鼠模型的特征在于人类突变的SOD1的过表达，通过形成细胞内蛋白质聚集体，引起兴奋性中毒，影响氧化平衡和干扰轴突运输而导致脆弱性增加。在这项研究中，我们跟踪了生物大分子有机物的组成和区划以及痕量金属的原位分布同时使用两种基于同步加速器辐射的方法将它们与ALS大鼠模型中的单个星形胶质细胞进行比较，并将其与非转基因同窝幼虫的对照星形胶质细胞进行比较：傅立叶变换红外光谱（SR-FTIR）和硬X射线荧光显微镜（XRF）。我们显示ALS细胞包含更多的铜，与总脂质共定位，增加的羰基和氧化的脂质，从而暗示了铜直接参与脂质组分的氧化应激而没有直接连接到蛋白质聚集的原位。

更新日期：2020-05-28

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