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吖啶橙对培养巨噬细胞溶酶体的光氧化损伤

Photooxidative damage to lysosomes of cultured macrophages by acridine orange.

作者信息

Zdolsek J M, Olsson G M, Brunk U T

机构信息

Department of Pathology II, University of Linköping, Sweden.

出版信息

Photochem Photobiol. 1990 Jan;51(1):67-76. doi: 10.1111/j.1751-1097.1990.tb01685.x.

Abstract

Cultured cells accumulate acridine orange (AO), which is a weak basic dye and a photosensitizer, in lysosomes and other acidic compartments. During exposure to blue light, AO-loaded macrophages show decreasing red granular fluorescence and increasing green diffuse fluorescence. This is hypothesized to represent peroxidative damage to lysosomal membranes resulting in an impaired proton gradient with deprotonation of the AO to its uncharged form and subsequent leakage of the dye. Further damage to the lysosomal membranes will result in release of lytic enzymes from the lysosomal compartment into the cytosol, leading to degeneration and finally cell death. The survival of AO-loaded and light-exposed macrophages is controllable by varying the exposure times to blue light. Inhibition of lysosomal proteases by E-64 results in increased cell survival after AO and blue light-mediated damage, indicating a role of proteolytic enzymes in this type of damage. Morphological analysis shows 'rounding up' with formation of retraction fibrils and pronounced plasma membrane blebbing. The formation of autophagic vacuoles is an early and pronounced event. After protease inhibition, however, all these phenomena are inhibitable to a considerable degree. We have thus directed photooxidative damage selectively to lysosomal membranes and their contents. This technique will allow further detailed studies of the role of lysosomes in degeneration-regeneration processes.

摘要

培养的细胞会在溶酶体和其他酸性区室中积累吖啶橙(AO),吖啶橙是一种弱碱性染料和光敏剂。在蓝光照射期间,负载AO的巨噬细胞会出现红色颗粒荧光减弱和绿色弥散荧光增强的现象。据推测,这代表溶酶体膜受到过氧化损伤,导致质子梯度受损,AO去质子化形成不带电荷的形式,随后染料泄漏。溶酶体膜的进一步损伤将导致溶酶体区室中的裂解酶释放到细胞质中,导致细胞变性并最终死亡。通过改变蓝光照射时间,可以控制负载AO并经光照的巨噬细胞的存活。E-64对溶酶体蛋白酶的抑制作用导致在AO和蓝光介导的损伤后细胞存活率增加,表明蛋白水解酶在这种类型的损伤中起作用。形态学分析显示细胞“变圆”,形成收缩纤维并出现明显的质膜起泡。自噬泡的形成是一个早期且明显的事件。然而,蛋白酶抑制后,所有这些现象在很大程度上都可被抑制。因此,我们已将光氧化损伤选择性地导向溶酶体膜及其内容物。这项技术将有助于进一步详细研究溶酶体在变性-再生过程中的作用。

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