Arsenic trioxide and ascorbic acid demonstrate promising activity against primary human CLL cells in vitro

被引：21

作者：

Biswas, Sabyasachi ^{[2
]}

Zhao, Xiaobin ^{[3
]}

Mone, Andrew P. ^{[2
]}

Mo, Xiaokui ^{[4
]}

Vargo, Melissa ^{[2
]}

Jarjoura, David ^{[4
]}

Byrd, John C. ^{[2
,4
,5
]}

Muthusamy, Natarajan ^{[1
,2
]}

机构：

[1] Ohio State Univ, Div Hematol & Oncol, OSUCCC, Columbus, OH 43210 USA

[2] Ohio State Univ, Dept Internal Med, Div Hematol & Oncol, Columbus, OH 43210 USA

[3] Ohio State Univ, Div Pharmaceut, Coll Pharm, Columbus, OH 43210 USA

[4] Ohio State Univ, Ctr Biostat, Columbus, OH 43210 USA

[5] Ohio State Univ, Coll Pharm, Div Med Chem, Columbus, OH 43210 USA

来源：

LEUKEMIA RESEARCH | 2010年 / 34卷 / 07期

关键词：

CLL; Arsenic trioxide; Ascorbic acid; CHRONIC LYMPHOCYTIC-LEUKEMIA; ACUTE PROMYELOCYTIC LEUKEMIA; GLUTATHIONE DEPLETION; INDUCED CYTOTOXICITY; INDUCED APOPTOSIS; MYELOID-LEUKEMIA; TOXICITY; LINES; PATHWAY; PEROXIDASE;

D O I：

10.1016/j.leukres.2010.01.020

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The compromised antioxidant defense system in chronic lymphocytic leukemia (CLL) suggested a potential use for reactive oxygen species (ROS) generating arsenic trioxide (ATO) and ascorbic acid. While both ATO and ascorbic acid mediate cytotoxicity in CLL B cells as single agents, the efficacy of ATO is enhanced by ascorbic acid. This effect is dependent on increased ROS accumulation, as pretreatment of B-CLL cells with a glutathione reducing buthionine sulfoximine or catalase inhibiting aminotriazole, enhanced ATO/ascorbic acid-mediated cytotoxicity. Pretreatment with reducing agents such as catalase, or thiol antioxidant, N-acetyl cysteine or GSH also abrogated ATO/ascorbic acid-mediated cytotoxicity. Furthermore, Hu1D10-mediated cell death was enhanced with ATO and ascorbic acid, thus justifying potential combination of ATO/arsenic trioxide therapy with antibodies such as Hu1D10 that also cause accumulation of ROS. (C) 2010 Elsevier Ltd. All rights reserved.

引用

页码：925 / 931

页数：7

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