Glucose toxicity in beta-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection.

By R. Robertson, J. Harmon, P. Tran, Yoshito Tanaka, H. Takahashi, P. Robertson. Diabetes, 2003

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beta-cell failure in diabetes and preservation by clinical treatment. (2007, background): “(47), if the steady decline in -cell function in DM2 is attributable to any significant extent to ongoing apoptosis via chronic oxidative stress with no deterioration in -cell replication, then interference with apoptosis by antioxidants or any other therapy, might provide a much needed new approach”
The role of oxidative stress in diabetic complications (2007, background): “Glucose, and many of its metabolites, can react with hydrogen peroxide in the presence of transition metals, such as Fe2+ and Cu2+, to form hydroxyl radical (•OH), the most reactive ROS (62,63).”
Diabetes associated cell stress and dysfunction: role of mitochondrial and non‐mitochondrial ROS production and activity (2007, background): “…C© 2007 The Physiological Society in β-cells compared to other tissues (Lenzen et al. 1996; Tiedge et al. 1997), β-cells are thought of as targets for oxidative stress-mediated tissue damage (Maechler et al. 1999; Tanaka et al. 1999; Evans et al. 2002; Tanaka et al. 2002; Robertson et al. 2003).”
Regulation of Insulin Synthesis and Secretion and Pancreatic Beta-Cell Dysfunction in Diabetes (2012, neutral): “Furthermore, there are elevated levels of oxidative stress markers in the blood and urine of T2D patients, and reduced glutathione (GSH) in blood cells [312].”