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Constant and intermittent high glucose enhances endothelial cell apoptosis through mitochondrial superoxide overproduction
Author(s) -
Piconi Ludovica,
Quagliaro Lisa,
Assaloni Roberta,
Da Ros Roberto,
Maier Amabile,
Zuodar Gianni,
Ceriello Antonio
Publication year - 2006
Publication title -
diabetes/metabolism research and reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.307
H-Index - 110
eISSN - 1520-7560
pISSN - 1520-7552
DOI - 10.1002/dmrr.613
Subject(s) - apoptosis , oxidative stress , nitrotyrosine , microbiology and biotechnology , overproduction , mitochondrion , oxidative phosphorylation , reactive oxygen species , chemistry , programmed cell death , superoxide , endothelial stem cell , mitochondrial ros , biology , biochemistry , nitric oxide synthase , enzyme , in vitro
Background It has been previously shown that hyperglycemia enhances free radical production, inducing oxidative damage, which in its turn activates the death pathways implicated in cell apoptosis and necrosis. But the possible involvement of this pathway in the hyperglycemia‐induced apoptosis of endothelial cells has not yet been reported. Methods To verify a possible connection between mitochondrial ROS production and apoptosis induced by both stable and oscillating high glucose, SOD, MnTBAP and TTFA was added to HUVEC cell culture medium. We measured nitrotyrosine and 8OHdG as oxidative stress parameters and Bcl‐2 expression and Caspase‐3 expression and activity as apoptosis indicators. Results Our results show that hyperglycemia, both stable or oscillating, increases oxidative stress and endothelial cell apoptosis through ROS overproduction at the mitochondrial transport chain level. Conclusion The prevention of mitochondrial oxidative damage seems to be a future important therapeutic strategy in diabetes. Copyright © 2006 John Wiley & Sons, Ltd.