PMID: 9003372Dec 15, 1996Paper

Reducing sugars trigger oxidative modification and apoptosis in pancreatic beta-cells by provoking oxidative stress through the glycation reaction

The Biochemical Journal
H KanetoN Taniguchi

Abstract

Several reducing sugars brought about apoptosis in isolated rat pancreatic islet cells and in the pancreatic beta-cell-derived cell line HIT. This apoptosis was characterized biochemically by inter-nucleosomal DNA cleavage and morphologically by nuclear shrinkage, chromatin condensation and apoptotic body formation. N-Acetyl-L-cysteine, an antioxidant, and aminoguanidine, an inhibitor of the glycation reaction, inhibited this apoptosis. We also showed directly that proteins in beta-cells were actually glycated by using an antibody which can specifically recognize proteins glycated by fructose, but not by glucose. Furthermore, fluorescence-activated cell sorting analysis using dichlorofluorescein diacetate showed that reducing sugars increased intracellular peroxide levels prior to the induction of apoptosis. Levels of carbonyl, an index of oxidative modification, and of malondialdehyde, a lipid peroxidation product, were also increased. Taken together, these results suggest that reducing sugars trigger oxidative modification and apoptosis in pancreatic beta-cells by provoking oxidative stress mainly through the glycation reaction, which may explain the deterioration of beta-cells under conditions of diabetes.

Citations

Feb 7, 2012·Free Radical Research·Qudsia Malik, Karl E Herbert
Jan 1, 2005·Toxicology Mechanisms and Methods·Raquel SeiçaMaria S Santos
May 1, 2007·Diabetes Research and Clinical Practice·Yoshifumi SaishoTakao Saruta
Sep 10, 2015·Pathophysiology : the Official Journal of the International Society for Pathophysiology·Adedayo O AdemiluyiMargareth L Athayde
May 6, 2004·Annals of the New York Academy of Sciences·Yoshitaka Kajimoto, Hideaki Kaneto
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Apr 12, 2006·The International Journal of Biochemistry & Cell Biology·Hideaki KanetoYoshimitsu Yamasaki
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