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细胞骨架的氧化变化导致特定细胞表面受体的改变。

Cytoskeletal oxidative changes lead to alterations of specific cell surface receptors.

作者信息

Malorni W, Rainaldi G, Rivabene R, Santini M T, Peterson S W, Testa U, Donelli G

机构信息

Department of Ultrastructures, Istituto Superiore di Sanità, Rome, Italy.

出版信息

Eur J Histochem. 1994;38 Suppl 1:91-100.

PMID:8547717
Abstract

Electron acceptors in biological systems, termed "oxidants", have been associated with numerous cytopathic conditions. In particular, oxygen-derived free radicals have been shown to induce various subcellular oxidative injuries which can lead to different types of pathologies. It has also been suggested that oxidative stress induced by xenobiotics can determine specific subcellular alterations in in vitro models. An oxidative imbalance in cells seems in fact to affect intracellular functions including the expression of some growth factor surface receptors. In this work, we observed a specific early alteration of the microfilament system and the microtubular network induced in K562 cells by oxidative stress. In particular, we hypothesize that oxidative imbalance could lead to an impairment of the expression of these receptors, such as transferrin receptors, via a modification of the cytoskeleton. This could represent a general mechanism by which a modification of receptor regulation can lead to cell aging, injury or death.

摘要

生物系统中的电子受体,被称为“氧化剂”,与众多细胞病变状况有关。特别是,氧衍生的自由基已被证明会引发各种亚细胞氧化损伤,进而导致不同类型的病理状况。也有人提出,外源性物质诱导的氧化应激可在体外模型中决定特定的亚细胞改变。事实上,细胞内的氧化失衡似乎会影响细胞内功能,包括一些生长因子表面受体的表达。在这项研究中,我们观察到氧化应激在K562细胞中诱导的微丝系统和微管网络的特定早期改变。特别是,我们假设氧化失衡可能通过细胞骨架的改变导致这些受体(如转铁蛋白受体)表达受损。这可能代表了一种普遍机制,通过这种机制,受体调节的改变可导致细胞衰老、损伤或死亡。

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