Literature DB >> 16453381

Constant and intermittent high glucose enhances endothelial cell apoptosis through mitochondrial superoxide overproduction.

Ludovica Piconi1, Lisa Quagliaro, Roberta Assaloni, Roberto Da Ros, Amabile Maier, Gianni Zuodar, Antonio Ceriello.   

Abstract

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.

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Year:  2006        PMID: 16453381     DOI: 10.1002/dmrr.613

Source DB:  PubMed          Journal:  Diabetes Metab Res Rev        ISSN: 1520-7552            Impact factor:   4.876


  95 in total

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