Session: MON 758-775-Beta Cells, Glucose Control & Complications
Poster Board MON-769
The cerebral pericytes were grown overnight in low glucose (LG, 5.7 mM) with or without mitochondrial carbonic anhydrases inhibitors, ethoxyzolamide or topiramate and then treated with high glucose (HG, 40.7 mM). Mitochondrial ROS was detected by treatment with MitoSOX followed by fluorescence imaging. The cell treated with high glucose showed an increase in mitochondrial ROS. Pretreatment with both ethoxyzolamide and topiramate significantly reduced high glucose-induced intracellular ROS overproduction. For the quantification a fluorimetric assay kit was used. A significant increase in ROS was reversed by pharmacological inhibition of mitochondrial carbonic anhydrases. The cell viability was unaffected by treatment with either ethoxyzolamide or topiramate.
These results provide the first evidence that high glucose induces excess mitochondrial ROS in cerebral pericytes, and pharmacologic inhibition of mitochondrial carbonic anhydrases attenuates high glucose-induced mitochondrial ROS in mouse cerebral pericytes.
Nothing to Disclose: TOP, ALRD, WAB, GNS
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