Hydroxyl free radicals generated by vanadyl[IV] induce cell blebbing in mitotic human Chang liver cells

被引：21

作者：

Bay, BH

Sit, KH

Paramanantham, R

Chan, YG

机构：

[1] Department of Anatomy, National University of Singapore, Kent Ridge

[2] Department of Anatomy, National University of Singapore, Kent Ridge

来源：

BIOMETALS | 1997年 / 10卷 / 02期

关键词：

confocal microscopy; glutathione; hydroxyl free radicals; scanning electron microscopy; vanadium;

D O I：

10.1023/A:1018331223538

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Vanadium has recently been reported to induce interphase and M-phase (mitotic) programmed cell death via the generation of hydroxyl free radicals (OH*). In this paper, the effects of antioxidants on: (a) vanadyl[IV]-generated OH* free radical levels; and (b) cellular glutathione in vanadyl [IV]-treated Chang liver cells were evaluated, The surface morphology of vanadyl-treated mitotic cells was studied by confocal and scanning microscopy. The free radical scavengers zinc chloride, glucose and thiourea reduced the levels of vanadyl-induced OH* free radicals and partially prevented the depletion of cellular glutathione. Concurrent with OH* free radical production, vanadyl-treated telophase cells exhibited excessive cell blebbing and cell shrinkage. The morphological features demonstrated in vanadyl-induced mitotic programmed cell death as a consequence of oxidative stress is novel.

引用

页码：119 / 122

页数：4

共 24 条

[1]

ARENDS MJ, 1991, INT REV EXP PATHOL, V32, P223

[2]

CHASTEEN ND, 1983, STRUCT BOND, V53, P105

[3] EXPOSURE TO LOW CONCENTRATIONS OF HYDROGEN-PEROXIDE CAUSES DELAYED ENDOTHELIAL-CELL DEATH AND INHIBITS PROLIFERATION OF SURVIVING CELLS [J].