In vivo amelioration of adriamycin induced oxidative stress in plasma by gamma-glutamylcysteine ethyl ester (GCEE)

被引:23
|
作者
Aluise, Christopher D. [1 ,2 ]
Clair, Daret St. [3 ]
Vore, Mary [3 ]
Butterfield, D. Allan [1 ,2 ]
机构
[1] Univ Kentucky, Dept Chem, Ctr Membrane Sci, Lexington, KY 40506 USA
[2] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40506 USA
[3] Univ Kentucky, Grad Ctr Toxicol, Lexington, KY 40536 USA
关键词
Adriamycin; Doxorubicin; Oxidative stress; Plasma; GCEE; Chemobrain; CENTRAL-NERVOUS-SYSTEM; LIPID-PEROXIDATION; PROTEIN OXIDATION; ALZHEIMERS-DISEASE; LIPOIC ACID; RAT-HEART; BRAIN; GLUTATHIONE; DOXORUBICIN; REPERFUSION;
D O I
10.1016/j.canlet.2009.02.047
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Adriamycin (ADR) is a common chemotherapeutic known to generate significant amounts of reactive oxygen species (ROS). Although ROS generation is one of several means by which ADR attacks cancerous tissues, oxidative stress-related toxicity has been documented in several non-targeted organs as a result of anthracycline chemotherapy. Oxidative damage to tissues has been shown in the past to be minimized with co-administration of various antioxidants. Gamma-glutamylcysteine ethyl ester (GCEE) is an antioxidant and precursor to glutathione that has been shown to successfully defend brain against ADR-induced oxidative stress. The current study shows ADR in vivo also causes oxidative stress in plasma in the form of protein oxidation [indexed by protein carbonyls and protein bound 3-nitrotyrosine] and lipid peroxidation [indexed by protein-bound-4-hydroxynonenal]. All three markers of oxidative stress are significantly suppressed with in vivo co-administration of GCEE. This work further supports the concept that administration of GCEE can protect patients undergoing anthracycline chemotherapy from non-targeted oxidative damage. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:25 / 29
页数:5
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