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Text
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URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2011.05.034" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2011.05.034</a>
Pages
876–883
Issue
4
Volume
51
Dublin Core
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Title
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Vitamin B12 protects against superoxide-induced cell injury in human aortic endothelial cells.
Publisher
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Free radical biology & medicine
Date
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2011
2011-08
Subject
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Aorta/pathology; Apoptosis/drug effects; Atherosclerosis/*drug therapy/metabolism/pathology/physiopathology; Cell Line; Cell Survival/drug effects; Cytoprotection; Endothelium; Free Radical Scavengers/*pharmacology; Humans; Mitochondria/drug effects/metabolism/pathology; Oxidative Stress/drug effects; Reperfusion Injury/*drug therapy/metabolism/pathology/physiopathology; Superoxides/metabolism; Vascular/*drug effects/metabolism/pathology; Vitamin B 12/*pharmacology; Vitamin B Complex/*pharmacology
Creator
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Moreira Edward S; Brasch Nicola E; Yun June
Description
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Superoxide (O(2)(*-)) is implicated in inflammatory states including arteriosclerosis and ischemia-reperfusion injury. Cobalamin (Cbl) supplementation is beneficial for treating many inflammatory diseases and also provides protection in oxidative-stress-associated pathologies. Reduced Cbl reacts with O(2)(*-) at rates approaching that of superoxide dismutase (SOD), suggesting a plausible mechanism for its anti-inflammatory properties. Elevated homocysteine (Hcy) is an independent risk factor for cardiovascular disease and endothelial dysfunction. Hcy increases O(2)(*-) levels in human aortic endothelial cells (HAEC). Here, we explore the protective effects of Cbl in HAEC exposed to various O(2)(*-) sources, including increased Hcy levels. Hcy increased O(2)(*-) levels (1.6-fold) in HAEC, concomitant with a 20% reduction in cell viability and a 1.5-fold increase in apoptotic death. Pretreatment of HAEC with physiologically relevant concentrations of cyanocobalamin (CNCbl) (10-50nM) prevented Hcy-induced increases in O(2)(*-) and cell death. CNCbl inhibited both Hcy and rotenone-induced mitochondrial O(2)(*-) production. Similarly, HAEC challenged with paraquat showed a 1.5-fold increase in O(2)(*-) levels and a 30% decrease in cell viability, both of which were prevented with CNCbl pretreatment. CNCbl also attenuated elevated O(2)(*-) levels after exposure of cells to a Cu/Zn-SOD inhibitor. Our data suggest that Cbl acts as an efficient intracellular O(2)(*-) scavenger.
Identifier
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<a href="http://doi.org/10.1016/j.freeradbiomed.2011.05.034" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2011.05.034</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2011
Aorta/pathology
Apoptosis/drug effects
Atherosclerosis/*drug therapy/metabolism/pathology/physiopathology
Brasch Nicola E
Cell Line
Cell Survival/drug effects
Cytoprotection
Department of Integrative Medical Sciences
Endothelium
Free radical biology & medicine
Free Radical Scavengers/*pharmacology
Humans
Mitochondria/drug effects/metabolism/pathology
Moreira Edward S
NEOMED College of Medicine
Oxidative Stress/drug effects
Reperfusion Injury/*drug therapy/metabolism/pathology/physiopathology
Superoxides/metabolism
Vascular/*drug effects/metabolism/pathology
Vitamin B 12/*pharmacology
Vitamin B Complex/*pharmacology
Yun June