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甲萘醌在哺乳动物细胞中的代谢所引起的表面形态改变与细胞骨架蛋白中关键巯基的氧化有关。

Alterations of surface morphology caused by the metabolism of menadione in mammalian cells are associated with the oxidation of critical sulfhydryl groups in cytoskeletal proteins.

作者信息

Mirabelli F, Salis A, Perotti M, Taddei F, Bellomo G, Orrenius S

机构信息

Dipartimento di Medicina Interna e Terapia Medica, University of Pavia, Italy.

出版信息

Biochem Pharmacol. 1988 Sep 15;37(18):3423-7. doi: 10.1016/0006-2952(88)90691-0.

Abstract

Incubation of freshly-isolated (rat hepatocytes) or cultured (HeLa, GH3, and McCoy) mammalian cells with menadione (2-methyl-1,4-naphthoquinone) resulted in the appearance of numerous cell surface protrusions. The perturbation of surface structure was associated with an increase in the amount of cytoskeletal protein and the oxidation of sulfhydryl groups in actin, leading to the formation of high-molecular weight aggregates sensitive to treatment with thiol reductants. Our findings indicate that the oxidation of thiol groups in cytoskeletal proteins may be responsible for menadione-induced cell surface abnormalities in mammalian cells.

摘要

将新鲜分离的(大鼠肝细胞)或培养的(HeLa、GH3和McCoy)哺乳动物细胞与甲萘醌(2-甲基-1,4-萘醌)一起孵育,导致出现大量细胞表面突起。表面结构的扰动与细胞骨架蛋白量的增加以及肌动蛋白中巯基的氧化有关,导致形成对硫醇还原剂处理敏感的高分子量聚集体。我们的研究结果表明,细胞骨架蛋白中巯基的氧化可能是甲萘醌诱导哺乳动物细胞表面异常的原因。

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