Kanwar M, Kowluru RA.
Wayne State University, Detroit, MI, USA.
Diabetes 2009;58:227–34.
Editor’s note: This article represents one step in a planned investigation of the basic science metabolic deficits that result in retinopathy in diabetes patients. Previous work by these investigators led them to examine the role of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a glycolytic enzyme that catalyzes the conversion of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate. They previously demonstrated that the GAPDH enzyme is inactivated by increased mitochondrial superoxide production and that this inhibition may activate some of the key pathways associated with diabetes complications, such as advanced glycation end products and activation of protein kinase C, as well as the hexosamine pathway. Therefore, in the current study, the authors quantitatively examined GAPDH enzyme activity, protein expression, ribosylation, and nitration using subcellular fractions of retinal tissue from rats with streptozotocin-induced diabetes.