Lack of mitochondrial depolarization by oxidative stress is associated with resistance to buthionine sulfoximine in acute lymphoblastic leukemia cells

被引：0

作者：

Goto, Hiroaki ^{[1
]}

Yanagimachi, Masakatsu ^{[1
]}

Kajiwara, Ryosuke ^{[1
]}

Kuroki, Fumiko ^{[1
]}

Yokota, Shumpei ^{[1
]}

机构：

[1] Yokohama City Univ Med, Dept Pediat, Kanazawa Ku, Yokohama, Kanagawa 2360044, Japan

来源：

LEUKEMIA RESEARCH | 2007年 / 31卷 / 09期

关键词：

acute lymphoblastic leukemia; glutathione; buthionie sulfoximine; oxidative stress; mitochondria;

D O I：

暂无

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Raised intracellular glutathione is one characteristics of high-risk childhood acute lymphoblastic leukemia (ALL). Depletion of glutathione by buthionine sulfoximine (BSO) has been reported to be toxic against some cancer cells. To assess the role of glutathione in ALL, the toxicity of BSO was studied in B-precursor ALL cell lines. BSO increased oxidative stress equally in all cell lines; however mitochondrial depolarization was observed only in BSO-sensitive cells. BSO up-regulated Bcl-2 protein, and antagonized the anti-ALL effect of prednisolone in BSO-resistant cells. A lack of mitochondrial death-signal activation by oxidative stress seemed to be associated with BSO-resistance in ALL. (c) 2007 Elsevier Ltd. All rights reserved.

引用

页码：1293 / 1301

页数：9

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