Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10882998 | Mitochondrion | 2013 | 6 Pages |
Abstract
Diabetes mellitus (DM) is associated with increased production of reactive oxygen and nitrogen species; consequently, an increase in lipid peroxidation and a decrease in antioxidants resulting in mitochondrial dysfunction. Using a rat model of DM induced by streptozotocin, we show the opposite: an increase in NO levels, S-nitrosylation, aconitase activity, and total glutathione and a decrease in lipid peroxidation at early stages of diabetes. These data imply that the decrease in lipid peroxidation is a vital early response to hyperglycemia to prevent escalation of ROS generation in mitochondria. These results also suggest a need for novel therapeutic targets to prevent the neurological consequences of diabetes.
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Biophysics
Authors
Ruth Noriega-Cisneros, Christian Cortés-Rojo, Salvador Manzo-Avalos, Mónica Clemente-Guerrero, Elizabeth Calderón-Cortés, Rafael Salgado-Garciglia, RocÃo Montoya-Pérez, Istvan Boldogh, Alfredo Saavedra-Molina,