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自体切割:氧化应激诱导癌细胞发生的另一种细胞死亡方式。

Autoschizis: another cell death for cancer cells induced by oxidative stress.

作者信息

Gilloteaux J, Jamison J M, Arnold D, Summers J L

机构信息

Department of Urology, Summa Health System, Akron, Ohio 44304, USA.

出版信息

Ital J Anat Embryol. 2001;106(2 Suppl 1):79-92.

Abstract

Scanning and transmission electron microscopy (SEM and TEM) were employed to characterize the cytotoxic effects of vitamin C (VC), Vitamin K3 (VK3) or a VC:VK3 combination on a human bladder carcinoma cell line (T24) following vitamin treatment. T24 cells exposed to VC alone showed membrane defects. VK3-treated cells show greater damage than VC treated cells because they exhibit membrane defects, cytoskeletal damage, excision of cytoplasm, and a substantial decrease in the number of viable cells. VC: VK3 treatment exacerbates the damages, especially intranuclear and nucleolar and induces an extreme reduction of cell size by cytoplasmic self-excision. Conversely, the nuclear envelope remains intact and the rough endoplasmic reticulum (RER) maintains its integrity until karyorrhexis occurs through a new phenomenon of cell death that we have named "autoschizis". From our morphological studies and previous biochemical reports on the topic, we are able to propose that this autoschizic cell death found is induced by oxidative stress.

摘要

采用扫描电子显微镜和透射电子显微镜(SEM和TEM)来表征维生素C(VC)、维生素K3(VK3)或VC与VK3组合对人膀胱癌细胞系(T24)进行维生素处理后的细胞毒性作用。单独暴露于VC的T24细胞显示出膜缺陷。经VK3处理的细胞比经VC处理的细胞损伤更严重,因为它们表现出膜缺陷、细胞骨架损伤、细胞质切除以及活细胞数量大幅减少。VC与VK3联合处理会加剧损伤,尤其是核内和核仁损伤,并通过细胞质自我切除导致细胞大小极度减小。相反,核膜保持完整,粗面内质网(RER)保持其完整性,直到通过一种我们称为“自切”的新细胞死亡现象发生核碎裂。根据我们的形态学研究以及之前关于该主题的生化报告,我们能够提出所发现的这种自切性细胞死亡是由氧化应激诱导的。

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